text:
Tool for translating chomosome, index numbers to sequence information
Is there a tool which allows me to transform information in the form (chromosome number, start index, end index) to sequence information? For example, something like (6, 43770819, 43770841) should yield GACCCCCTCCACCCCGCCTCCGG as this is the relevant bases on the 6th chromosome.
A command line executable is preferred, although a web-based service is also fine. Thanks a bunch in advance.

I think this should be possible with Biomart.

You can write a small script to do that. Basically you just have to print a string from position-x to position-y. Explaining how to do that is not really on-topic here.
From available tools you can use getfasta from the bedtools package. This requires a BED file, or a GTF file  as an input. The three column format as in your question will also work but usually the orientation (+/-) is also important to fetch the right sequence; otherwise all sequences would be fetched from the + strand only. GTF format is a bit different: the three columns in your question would be the first fourth and fifth column in the GTF. Seventh column holds the orientation.
bedtools getfasta [OPTIONS] -fi <input FASTA> -bed <BED/GFF/VCF> -fo <output FASTA>

(or):
getFastaFromBed [OPTIONS] -fi <input FASTA> -bed <BED/GFF/VCF> -fo <output FASTA>

There is another one called gffread which comes with the tophat package.
gffread takes a GTF/GFF file as an input and gives you a fasta file of sequences corresponding to the positions listed in the GTF file. The third column (feature) should be exon or transcript as this tool was actually designed to extract transcript sequences.
gffread -w transcripts.fa -g /path/to/genome.fa transcripts.gtf


text:
Why are some genomic regions sequenced more than the others?
We have to normalise read count data from RNA-Seq experiments in order to account for the fact that some genomic regions are mapped more than others. i.e. we get the tags per million reads (TPM). In other words, they have a higher sequencing depth/vertical coverage.
Why are some genomic regions mapped more than others; what is the reason for this non-uniform distribution of sequencing depth?

For RNAseq, the differences in the read depth can simply arise because of expression (that's trivial). Highly expressed regions will have higher number of reads.
However the read depth non-uniformity also arises because of the nucleotide composition of the regions. This is true for all kinds of nucleic acid sequencing such as RNAseq, whole genome sequencing and ChIP seq. This is called sequence bias. This also depends on the sequencing methodology. A variety of factors play a role such as how well can the region be sheared, how well can it be amplified etc.
For details have a look at this article by Ross et al (2013).

Sequencing technologies are vulnerable to multiple sources of bias.
  Methods based on bacterial cloning and Sanger-chemistry sequencing [8]
  were subject to many coverage-reducing biases, notably at GC extremes,
  palindromes, inverted repeats, and sequences toxic to the bacterial
  host [9–17]. Illumina sequencing [18] has been shown to lose coverage
  in regions of high or low GC [19–22], a phenomenon also seen in other
  'next-generation' technologies [3, 6]. PCR amplification during
  library construction is a known source of undercoverage of GC-extreme
  regions [20, 21] and similar biases may also be introduced during
  bridge PCR for cluster amplification on the Illumina flowcell [23].
  Illumina strand-specific errors can lead to coverage biases by
  impairing aligner performance [24]. Ion Torrent [25], like 454 [26],
  utilizes a terminator-free chemistry that may limit its ability to
  accurately sequence long homopolymers [4, 27, 28], and may also be
  sensitive to coverage biases introduced by emulsion PCR in library
  construction. Complete Genomics [29] also uses amplification along
  with a complex library construction process. The Pacific Biosciences
  [30] process is amplification-free; therefore, one might expect it to
  exhibit lower levels of coverage bias than the other technologies.
In addition to sources in the wet lab, bias can be introduced by any
  of the computational steps in the sequencing pipeline.
  Signal-processing and base calling limitations could result in
  under-representation or increased error rates in some locations, as
  can inaccurate alignment. An inaccurate reference or sample-reference
  differences can cause coverage or accuracy variations that may be
  misdiagnosed as sequencing bias. Therefore, detecting bias is only the
  first step and must be followed by more detailed experiments to assign
  responsibility to the library preparation, sequencing, or
  computational stages.

Some analysis software try to correct for these biases while estimating the read abundance.

Ross, Michael G., et al. "Characterizing and measuring bias in sequence data." Genome Biol 14.5 (2013): R51.

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text:
Movement in microvilli
My textbook( COMPREHENSIVE TEXTBOOK OF PHYSIOLOGY VOL-1 by GK PAL) says:

Microfilaments project into microvilli present on the epithelial surface such as on the intestinal mucosa, and extend up to the tip of microvilli. They help in microvilli movement.

How far is the second sentence correct? When I searched on Wikipedia( in a page about microvilli) I found following:

As mentioned, microvilli are formed as cell extensions from the plasma membrane surface.Actin filaments, present in the cytosol, are most abundant near the cell surface. These filaments are thought to determine the shape and movement of the plasma membrane.

So does these two imply that there is some sort of movement (due to actin) in microvilli?

Just the presence of actin filaments does not mean a cellular structure that contains it would be dynamic. Moreover there are different types of actin filaments (filopodia, lamellipodia etc) and they have different dynamics.
Microvilli closely resemble filopodia; both these structures also share some regulatory and structural proteins (other than actin). However, there are some differences which makes filopodia highly dynamic in comparison to microvilli (Sebé-Pedrós et al., 2013; Sauvanet et al., 2016).
Microvilli, though not as dynamic as filopodia, are not static structures. They can grow and retract and there are regulatory mechanisms that govern these processes (Sauvanet et al., 2016).

REGULATION AND DYNAMICS OF MICROVILLI AND MICROVILLAR COMPONENTS
Microvilli on cultured cells are dynamic structures with three phases
  in their life cycle: (a) the generation of microvilli growing at 5
  nm/s, (b) a steady state of ∼5 min, and (c) a retraction phase with a
  rate of 1.2 nm/s (Gorelik et al. 2003). This leads to an average life
  cycle of 12.1 ± 5.6 min. The turnover of microvillar proteins has been
  recognized for a long time (Stidwill et al. 1984). The F-actin core in
  the microvilli of Caco-2 cells at steady state treadmills, with a rate
  of monomer addition at the barbed end of approximately 1.5–3.0
  s−1 (Loomis et al. 2003, Tyska & Mooseker 2002),
  corresponding to approximately 0.2 μm/min. The protocadherin
  intermicrovillar link stabilizes microvilli of intestinal epithelial
  cells, resulting in a prolonged steady state (Crawley et al. 2014).
  The actin filaments in the core of stereocilia treadmill more slowly,
  at 0.002–0.04 subunits s−1 (Rzadzinska et al. 2004) or
  hardly at all (Zhang et al. 2012).

so does the movement implies growth and retraction?

@JM97 yes. It is pretty much evident from the quoted text. For more details you can check out the article.

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text:
What is Pseudopalindrome?
I stumbled upon this word in a webpage by bio.libretexts.org:

The dam-methylase of E. coli recognizes the tetranucleotide GATC in DNA and transfers a methyl group (from S‑adenosyl methionine) to the amino group at position 6 of the adenine in that sequence. Note that GATC is a pseudopalindrome, so both strands read the same for these four nucletides in DNA.

What does it mean? How is it different from palindromic sequence?
I've searched google,ncbi and google.books but couldn't find anything.

Please rephrase the title of your query, so that it actually reads and appears like a question.

'True' palindromes read the same from 5' to 3' as 3' to 5' on the same strand. Pseudopalindromes read the same as their reverse complements.

@Galen What is reverse complement?

@SanjuktaGhosh 1. Reverse order of characters (GATC ->CTAG); 2. Find complement strand (CTAG -> GATC). Note for this particular (pseudopalindrome) sequence, the steps invert each other.

Try this app to get a feel for what is happening in reverse complementation: http://www.bugaco.com/calculators/dna_reverse_complement.php

If you have Shell or Shell-like terminal, try playing around with: (tr ACGT TGCA | rev) <<< 'input_seq'

I believe a main problem here is that the quoted text is not using the term 'pseudopalindrome' in a biological-jargon sense. Unfortunately, molecular biology does not use 'palindrome' in the normal sense, but in a sense that directly contradicts the normal sense. A normal palindrome formed from GA would be GAAG, but a bio palindrome formed from GA would be GATC.

In DNA there are four nucleotides or "bases", each of which can be matched with a complementary base on the partner chain in the double helix. Thus:
Adenine (A) and Thymine (T) are complementary and Cytosine (C) and  Guanine (G) are complementary.
So, a nucleotide sequence is said to be a palindrome if it has an even number of base pairs and is equal to the reverse of its complementary sequence.
For example, in a single strand of DNA the sequence of bases CCATTAATGG is palindromic because the sequence of bases in the complementary strand is GGTAATTACC, its reverse.
A pseudopalindrome is a DNA sequence with an odd number of base pairs yielding a symmetrical complement except at the central base-pair. For example, the DNA sequence ACCTGGT is pseudopalindromic, because its complement on the other strand is TGGACCA, which is its reverse except for the central element.
[There may be some confusion in the literature. The example cited in the question, GATC, is a palindrome, having CTAG as its complement, not a pseudopalindrome.]

Some of the papers I found also portrayed in your direction. Could you provide a link that I can check out?


text:
What are housekeeping and constitutive genes?
I have come across two set of definitions which are not contradictory but different.
From wikipedia:

A constitutive gene is a gene that is transcribed continually as opposed to a facultative gene, which is only transcribed when needed.
A housekeeping gene is typically a constitutive gene that is transcribed at a relatively constant level. The housekeeping gene's products are typically needed for maintenance of the cell. It is generally assumed that their expression is unaffected by experimental conditions. Examples include actin, GAPDH and ubiquitin.

My question from these definitions: What does 'transcribed at a relatively constant level' mean? Does it mean that a constant level of gene product is maintained in a cell? I can't understand there meanings atal.
Again,according to Oxford dictionaries

Constitutive Genes are genes that are expressed following interaction between a promoter and RNA polymerase without additional regulation.
  (Oxford Dictionary of Biochemistry and Molecular Biology)
Housekeeping genes - Constitutive loci that are theoretically expressed in all cells in order to provide the maintenance activities required by all cells: e.g., genes coding for enzymes of glycolysis and the  and the citric acid cycle.(Dictionary of Genetics)

These definitions do not tell whether they are continually transcribed or the synthesised products are present in constant amount.
Which one best define them?

I don't really understand your question. What part of the quoted definitions confuses you?

I think you missing gene expression logic here. There are promoters that require transcription factors to start producing gene. In other words, housekeeping genes only require their DNA + RNApol to produce mRNA. Non-housekeeping genes require their DNA + RNApol + SomeOtherFactors (proteins)

@canadianer I've edited the content.

@BryanKrause You should post that as an answer. I would only add that transcription initiation is not the only level of gene regulation. Constitutive transcription need not imply that that protein levels will continually rise since that is also influenced by the rate translation and protein/mRNA degradation.

@canadianer Thanks, I'll include that important point in a brief answer and remove my earlier comment.

I think the best answer is both: they are continually transcribed at a rate that maintains the synthesized products at a (roughly) constant level. These terms are really just descriptive terms, there is no true biological dichotomy, it's just that some genes are expressed pretty much all the time and others are only produced when needed, for example genes for proteins needed at a particular stage of the cell cycle.
As @canadianer mentions in a comment, there are also other forms of post-transcriptional regulation, such that constitutive transcription doesn't necessarily mean constant production of protein at an equal rate.
Wikipedia has quite a list of different "housekeeping genes" and you will see the list is quite extensive. It certainly isn't true that all of these genes are expressed at exactly the same levels all the time, it is simply that their expression is consistent enough to be used as an approximate standard when comparing expression levels.
If I could produce a definition that reflects reality better than the ones you found, I would amend the Oxford definition to something like:

Constitutive Genes are genes that are expressed following interaction between a promoter and RNA polymerase at a level that doesn't seem to vary much across cells of the same type, doesn't require a very special transcription factor, and so far biologists haven't found an experimental condition that greatly impacts the expression level.

The questioner asks “What does ‘transcribed at a relatively constant level’ mean?” The answer is absolutely nothing!
A gene can be transcribed at a constant rate, or maintained at a constant level (in so far as ‘level’ — a word that should be avoided — is taken to mean ‘amount’). Perhaps it means ‘transcribed so as to maintain a relatively constant cellular concentration of the product’. It is unclear.
I’m afraid that it is a waste of time trying to find an authority for definitive meanings for terms that were coined in a period of incomplete scientific knowledge and have changed their meaning or importance as science has progressed and time has passed. Wikipedia is written by anyone who cares to contribute and its authority tends to vary with the amount of interest experts in the field have. For computing science you are on a winner, for molecular biology you may not be.
As far as the term housekeeping gene goes, a Google ngram shows that it appeared about 1980, at a time when little was known about the regulation of the expression of eukaryotic genes. The term expressed the simplistic idea of genes that were expressed continually (as in the examples quoted) as opposed to those induced by particular stimuli like sexual differentiation or perhaps change in diet. In fact little was known about inducable genes at the time, and the concept was very much based on an analogy with bacterial systems, which are different in many ways. It is still useful in a general sense, but no more.
PS
I've edited the Wikipedia entry. We'll see if anyone cares. (I can edit it, but anyone else can switch it back to the original. In that case it is best discussed.)

+1 for pointing out a key point that I glossed over in my answer: these terms are somewhat outdated, even if they are still in use. They really don't have a lot of useful relevance to our current understanding of biology. Sadly textbooks and curriculum are a bit behind the times, in part because its so hard to keep up with the pace of scientific discovery.


text:
Contact Inhibition of Cell Division: Signaling Pathway
The following article refers to contact inhibition of cell division in epithelial cells, specifically MDCK cells: Collective and single cell behavior in epithelial contact inhibition.
In their review of the literature, there are a number of possible signalling pathways implicated in contact inhibition of cell division. These pathways are outlined in the following quotes:

It is widely accepted that contact inhibition requires establishment of E-cadherin-mediated cell-cell contacts and subsequent maturation of the adherens junctions (AJs) that link E-cadherin and F-actin in a synapse-like complex involving numerous other proteins
One possible pathway involves β-catenin, a mediator of Wnt signalling, that, in addition to its function as a transcriptional cofactor, is associated with the AJs at the cell surface
A contact inhibition role has been reported for NF2/Merlin, a tumor suppressor gene that encodes a membrane-cytoskeletal scaffolding protein, which most likely acts via the Hippo kinase pathway, controlling nuclear localization of the transcriptional activator YAP—itself a known regulator of cell proliferation.
Contact inhibition is known to involve the MAPK pathway, which, in turn, promotes cell cycle entry by regulating the expression of cyclinD1. Also implicated are Nectins—a family of cell adhesion molecules that are involved, together with integrins and other proteins, in the regulation of cell motility and proliferation. Yet, this accumulated knowledge falls far short of a comprehensive picture of contact inhibition.

In the article, the findings were as follows:

Our findings show that contact between cells is not sufficient for inhibition of mitosis in MDCK cells. Instead, inhibition of cell proliferation is a consequence of mechanical constraint that causes successive cell divisions to reduce cell area.

Where, in the discussion, they note the following:

Our measurements also suggest that inhibition of cell division is a distinct single cell state rather than a global state induced by cell-cell signalling across the layer, as illustrated in Fig. 4E. In fact, confluent MDCK cell cultures with an average cell density corresponding to the morphological transition are often sufficiently heterogeneous in local cell density that highly motile cells and completely arrested cells coexist in the same colony. Thus contact inhibition is a local phenomenon...

Published later, the article Spatial constraints control cell proliferation in tissues showed that reducing the amount of space in a tissue prevented entry into S-phase. Actually stretching the tissue quickly reactivated the cell cycle, and compression leads quickly to arrest. More so, they found that cells had no memory of past constraint, and were able to suggest a model of growth in relation to the spatial constraint.
I'm editing my question because the way I posted it initially, to me, was unanswerable. Being said, I suspect that at this point cell volume and extracellular contacts are synergistic. This is probably going to need two separate questions, but:
1) How does the mitotic entry machinery roughly respond to cell volume? I'm currently reading into Cdc25/Wee1 regulation in addition to some stuff about internal fluidics that are influenced by water, ion channels, etc. but I still don't fully understand.
2) What's a relatively straightforward downstream pathway (core elements), starting at the adherens junctions, that illustrates how cell-cell signalling gets the STOP signal to the mitotic entry machinery (based on what we know)? This might require some much more in-depth knowledge about the field, however, but articles with some good figures are appreciated, too.

As far as I know our knowledge is incomplete. We understand some pathways involved (notably MAPK) but don't really understand the interactions between pathways. As an example the AMPK and MAPK/ERK pathways share common downstream molecules and have some positive/negative feedback loops which are hard to model (I know I tried to model the ERK one) as we don't know all the involved players and the interactions between them. As an example in the MAPK/ERK pathway MEK can self-dimerize which was discovered late last year and actually this provokes a buffering effect on the response.

Agree that we don't really know. I think that you might gain some perspective by looking at related pathways, e.g. effect of mechanical forces on mitotic spindle orientation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169662/. I believe there is a lot of work in Drosophila on this subject, cursory googling suggests that preferential elongation along a particular tissue axis is mediated by mechanical forces: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0086725, using the wing as a model.

How does the mitotic entry machinery roughly respond to cell volume?

This is a broad question but luckily there is one article that addresses this precise question in detail. However, it is very likely that more discoveries are made on this topic in future.
Neurohr et al. (2019) have extensively studied the effect of cell volume on mitotic re-entry and cell cycle progression. They used Saccharamyces cerevesiae with temperature sensitive alleles of CDC28 to arrest the cells in G1 phase. At this stage high glucose concentration (2%) led to increase in cell volume compared to that of starved (0.1% glucose) or protein synthesis inhibited (2% glucose + cycloheximide) cells. Using this model they find that cytoplasmic dilution causes impairment of transcriptional regulation during cell cycle progression. This is because the transcription factors do not scale with cell size.
Read the paper for more details.

What's a relatively straightforward downstream pathway (core
  elements), starting at the adherens junctions, that illustrates how
  cell-cell signalling gets the STOP signal to the mitotic entry
  machinery?

This is again a broad question if you expect all details. However, google scholar search on "contact inhibition pathway" suggests that the main downstream pathway is the Hippo signalling pathway.
Top hits on this topic:

Zeng, Qi, and Wanjin Hong. "The emerging role of the hippo pathway in cell contact inhibition, organ size control, and cancer development in mammals." Cancer cell 13.3 (2008): 188-192.
Kim, Nam-Gyun, et al. "E-cadherin mediates contact inhibition of proliferation through Hippo signaling-pathway components." PNAS 108.29 (2011): 11930-11935.
Gumbiner, Barry M., and Nam-Gyun Kim. "The Hippo-YAP signaling pathway and contact inhibition of growth." J Cell Sci 127.4 (2014): 709-717.

Huuuuh I'll admit this question was really broad at the time but that first article, well one I've become so busy it dropped off my radar, but I also didn't expect those conclusions either. I will need to research the latter half better, but thanks for a point in the right direction!

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text:
How often does bacterial transformation happen?
I have been reading:

M. Dröge, A. Pühler, W. Selbitschka, "Horizontal gene transfer among bacteria in terrestrial and aquatic habitats as assessed by microcosm and field studies", Biol. Fertil. Soils (1999) 29 pp221–245  [PDF]

I am not a biologist and am trying to get a feeling for how often prokaryotes make changes to their chromosomal DNA.
How often is plasmid DNA successfully incorporated into chromosomal DNA?
I would like to estimate either the number of gene changes (or, failing this, base pair changes) that a bacterium makes per unit time. Or, equivalently, the mean time between such changes.

Transformation underpins a lot of lab modern projects.
This will be a very unsatisfying answer, and this wikipedia entry explains why. The time, and success, of bacterial transformation of competent cells varies greatly depending on a few things mainly:

the length of nucleic acid sequence for insertion (or more accurately, the plasmid)
the species of target organism (or more accurately, the genotype of the target organism)
a host of other things

With a specific plasmid and organism you would be able to get a more satisfying answer, but I imagine the answer would even differ from lab to lab.
I worked with a microbiologist that provided me with a protein as a part of my honours project, and I can give you a broad impression I got from them: it does not happen often. Sometimes none of the cultures you are trying to transform will incorporate the new sequence into their genome, other times the cloning process goes very well and all your cultures will be transformed successfully. For our project, valid colonies only presented after a week with reasonable success (more than half the attempts were successful). But you don't know if the transformation worked until way after the first transformation happened.
The mechanisms behind this are grossly understudied. If we take some thing B. subtilis, arguably the most academically studied organism in the field of transformation, it can take up the DNA as food or incorporate it into its genome but nobody knows exactly how this happens at a molecular level (Chen & Dubnau, 2004)

Chen, I., & Dubnau, D. (2004). DNA uptake during bacterial transformation. Nature Reviews. Microbiology, 2(3), 241–9

Thanks, this is fantastic! I mean, it's not a satisfying answer as you say, but it is great to hear from someone who has some qualifications in the field. My lay impression too was that these things were greatly understudies. Many thanks again!


text:
What is the location of the Hypoglossal nerve?
I kind of know where the hypoglossal nerve is located when I look at the diagram, but I'd like to know how far is the nerve from the skin and where is the closest area to the skin before and right after it's branching?
Is there any video or schema showing the location of the Hypoglossal nerve relative to skin and not the skeleton?
From this pic. I can't really tell the closest location of being able to detect the nerve near the skin.

I found a video of a surgery on youtube where the surgeon locates both the facial nerve and the hypoglossal nerve. It is a surgery so I "warn" you before clicking the link. https://www.youtube.com/watch?v=_5brqIa_KLk

The following image of a cadaver shows the hypoglossal highlighted:

 Source: StudyBlue
You can see the flap of skin/muscle that has been removed to get an understanding of the thickness of tissues separating the nerve from outside the body.
Additionally, here is an image showing a person receiving an operation. You can see the relative depth of the nerve fairly well:

 Source: Cambridge University Press


text:
What is membrane-partitioning free energy? Can it be simulated?
Firstly, is there a strict definition of the "membrane-partitioning free energy"? It is banded around in membrane biology, but I have never seen it strictly defined. The only non-scholarly site that google shows is this Q&A on quora, and the answer there even has ambiguity in what is defined as partitioning in the membrane. This seems wholly unclear.
Furthermore, is it possible to study free energy changes upon partitioning in GROMACS, or with any other molecular dynamics simulations? If not, what are the methods I would need to use to determine the free energy of partitioning?
Links and citations for further reading on this topic are encouraged.

Welcome to Bio. Could you add some bacground to your question? The sources for the terms would be of help. For example, what membranes are you talking about? What are the purposes of the methods you are looking for? Good answers can only be generated to clear questions.

When you refer to membrane partitioning, are you referring to the invagination of the membrane during cytokinesis or do you have something different in mind?

In the biological context, membrane-partitioning is usually referring to the stage in which the transmembrane-destined region of a protein moves from interacting with the water, to interact with the interface of the membrane.
In the diagram below showing a four step thermodynamic cycle, the partitioning free energy can be referred to as-is ΔGwiu in terms of free energy where w is water, i is the interface, and u is unfolded. The image comes from the same paper that introduced the famous Wimley and White octanol-interface scale from 1999.

Note that in a more recent 2015 article, they comment that the partitioning phase ΔGwiu is generally the only experimentally accessible step. With that in mind, simulating ΔGwif where f is the folded helix becomes necessary. This 2014 Nature Comms paper use folding-partitioning molecular dynamics simulations to estimate the free energies that are experimentally inaccessible. They used Gomacs 4.5. In fact, a study using a simulation from 2005 suggests that folding isn't necessarily required for insertion of the helices.

Note that all the information here is behind a paywall. Feel free to ask me for clarification or expansion in the comments.

James, pm me. Would love to hear more from you in this subject.

@RoshanShrestha Ping me in the biosphere, or via twitter (@jbkr_). There is no PM function I'm aware of here.


text:
Programmatic way to differentiate homodimers from heterodimers?
For pdb files is there a simple programmatic way to determine if the file is made up of homodimers or heterodimers.
I have many files so an online tool or some psuedocode/scripts would help more than manually assessing each one.

Could you provide us with an example? Preferably one that is a homodimer and one that is a heterodimer.

I don't think this post deserves closing. I have tried to tidy up the question so its easier to understand. Correct me if I am wrong, but is OP asking if there is a programatic way to check if in a dimer both monomers are either the same or different?

Have you tried simply checking the sequences? same sequences for proteins = homodimer... I have distant memories of pdb fileformat, but as far as I remember individual protein chains are stored separately, but I may be dead wrong on this one.

How comfortable are you with scripting?

There was a recent discussion on this sort of question in meta. What you're asking here is not actually about biology, but about programming. Furthermore, as it stands this question could be interpreted as a "give me the codes" question. What have you tried so far?

In case you want to write your own subroutine,
1. Scan the whole .pdb file for number of chains present, if multiple then proceed.
2. Create index_counter for each amino acids of a single chain.
3. Now, For SINGLE chain. While you scan for each amino acid perform a i=i+1 operation for that specific amino-acid_counter.
4. Compare the amino-acid_counter between/among the chains.
5. Exact match = homomer or non-exact match = heteromer.
Hope you get the logic.

I think you will run into trouble with real live PDB-files here - often there are gaps in the sequence because they were not observed in the electron density, or the numbering is inconsistent. I would suggest to rather extract the sequence from the PDB-file and align them (eg using fasta).

@Gerhard yeah! but that depends on how good is the resolution and R-free value of your .pdb is. When you are talking about analyzing .pdb you are supposed to take a higher resolution <1.6A. This covers all the atoms vwd radii(except H), no atom-missing issue is possible. Literature says.

A) if you limit yourself to anything better than 1.6A, there are not many structures left, and (according to Murphy) most likely not the proteins you are interested in. B) whether you have gaps and missing parts in a crystallised molecule is not necessarily down to resolution and Rfree (although there is a correlation). Some parts of a molecule - in particular loops - are simply more flexible and hence disordered in the crystal - no resolution in the world will make these appear.  C) Could you post the reference you mentioned - quite interesting as a crystallographer.

It's a general methodology as reported in every data-mining literature, that's why I emphasized on resolution. And as per my experience, I found that if you have a higher resolution, then random coils(most of the time) shows fluctuating occupancy, but still be present. Although you are right, some gaps stays sometimes(specially in multidomains proteins). However the subroutine can be configured to eliminate any structures with breaks and analyze further. But to reach publication quality I think high-res is always needed. -  it's always nice to see a crystallographer around.

I'd just compare the amino acid sequences of the individual protein chains. With some leeway for residues not observed in the density, ie only require 90 or 95% sequence identity, or ignore gaps.
This will not tell you anything about whether the dimer (if you observe several molecules in the asymmetric unit) is actually real. For that, you'd need to do an experiment, literature research or see whether software like the PISA-server could give you a clue.


text:
Why do negative ions flow into a cell in an inhibitory synapse, even though a neuron has a negative resting potential?
In my spare time I have been reading an introductory Psychology textbook and this question came to my mind after reading about action potentials.  I have no previous knowledge in chemistry so if I do need some sort of other knowledge I would appreciate if I could be told what I need to learn in order to understand the physiology of the nervous system better. So Why do negative ions come into a cell during an inhibitory synapse even though a neuron has a negative charged resting potential?
I understand this question might be extremely vague and impossible to answer without previous knowledge of the physiology of the nervous system. Any help would be greatly appreciated.

Welcome to chemistry.SE! I reckon this is perfectly on-topic here, but is there a reason you didn't ask this on Biology.SE? A better understanding of the workings of nervous system could lead to better answers.

Oh sorry about that.  I wasn't aware about a biology section.  I literally just found out about this website so i'm extremely nooby.

Welcome to Biology! I see that @Jonsca rightfully migrated your interesting question to us. I have made some slight edits to your question, feel free to roll back if it is not to your liking.

Short answer
Negative ions can flow against the electrical gradient into the cell, provided their concentration gradient across the cell membrane is large enough.
Background
When an ion channel opens, the resultant ion flow is dependent on two things; the membrane potential (which is indeed negative at rest) and the concentration gradient of the ion.
Consider the activation of a GABAA receptor. GABA is the principial inhibitory neurotransmitter in the nervous system. GABA opens the associated Cl- channel on GABAA receptors.
Using the Nernst equation one can approximate the membrane potential (Veq) at which an ion is in equilibrium. It mainly depends on the concentration of the ion X outside and inside the cell ([X]o and [X]i, respectively).[Cl]o is approximately 103 mM, and [Cl]i 4 mM. Hence, there exists a large concentration gradient with lots of it outside the cell.

Nernst equation. Source: Physiology Web
In a neuron, the Nernst potential of Cl- is around -71 mV. Hence, given that the resting membrane potential is approximately -70 mV for a typical neuron, no Cl- flux will occur when Cl- channels open, because the resting membrane potential is equal to the equilibrium potential of Cl-. However, when a neuron is depolarized by stimulatory neurotransmitters (e.g., glutamate), the membrane potential may be reduced to, say, -60 mV. This is still more negative than the action potential threshold (about -55 mV), but very close to it. So without any inhibition the neuron would be close to firing a spike. However, when GABA is released presynaptically, opening of the Cl- channels coupled to GABAA receptors will result in Cl- influx, because the membrane potential is higher (more positive) than the equilibrium potential of Cl-. In effect, Cl- will enter the cell until its equilibrium potential is reached, re-polarizing the neuron back to -70 mV and hence inhibiting it.

Wow thank you so much for your detailed answer!

@user16831 - my pleasure! I hope my answer did not get too technical. I see you are just getting comfortable in this area of science. Also, considering you are new - you can vote on any answers you receive by using the up/down vote buttons. You may accept an answer by clicking the check mark. However, you don't have to user the voting system. It's up to you :)

I had to read it a few times but I like details haha :)

I can't add any detail to AliceD's answer, but I can put it in different terms, and perhaps that could be helpful to you.
Yes, Cl- ions are negatively charged, and the neuron is very often negatively charged. Given only those two facts, yes, you would think Cl- would not enter the neuron. But there is another key fact: diffusion.
The Cl- ions feel the force of electrical repulsion, but since they are at body temperature they also feel the force of slamming into each other at very high speeds and bouncing every which way. This "slamming force" tends to spread them out, and that is otherwise known as diffusion. Since there are many more of them outside the neuron than inside (due to active pumping them to that imbalanced state), the force of diffusion tends to drive them inside the neuron--at least as long as it's not too negative in there! If it is too negative, then no, the force of diffusion is not enough to push the Cl- ions into the neuron, and in fact they may leave the neuron.
What I've written here is, I think, (essentially) equivalent to AliceD's fine answer.

Afaik, chloride ions are not actively pumped out of the cell.

@AliceD http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282916/ as an example.


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Teens concerned about impregnation through clothes
Dry Humping, is:

dry humping is the process of two people repeatedly moving up and down and back and forth on top of each other fully clothed( or missing various pieces, but the penis must not come in contact with the vagina with out some sort of fabric separating them ex: boxers,panties, or even sheets!!)

We all know that the basic rule for impregnation is that the sperm must come in contact with the egg, and even be able to fertilize it. While sperm can get through clothes, semen (but this is yet been proven or disproved) gets stuck, thus the sperm dies.
What is your opinion about this? If two people are on top of each other, fully clothed, and the male comes to ejaculation, is there any chance that pregnancy can happen, in the realistic and biological look at it (and not some probability or statistical way)? What advice should be given to teens on the matter?
I am a computer scientist with no biology knowledge, and am very interested in getting the opinion of biologists.
But since I know that the stackexchange community likes to see work done before asking questions, I did my own research (I am used to googling code and algorithms):
Very few research has been done on the subject. There is one shining research that  concluded, as I recall, that:

If the underwear is completely saturated with semen, and is in direct contact with the woman's vagina, pregnancy is possible statistically, but highly unlikely.

If there has been an ejaculation by the male, and semen is present, there is a chance of getting pregnant. Period. Teens really need to know that.
I think you may have your terms confused - semen is the overall fluid released during an ejaculation, sperm are the cells with tails that are produced in the testes and fertilize the egg. At any rate, according to the WHO, a normal sperm count is over 15 million per milliliter, with some counts much higher (>50e6/ml ), and an average between 20 and 40 million. The volume of the ejeculate tends to be anywhere from 1-6 ml. If you take a healthy young male at the peak of his reproductive capabilities, this equates to a very large number of sperm being released during a sexual encounter. All it takes is for one to reach an egg and fertilize it. Sperm are very very small, much smaller than the pore size of average fabric, so clothing will do very little to stop them. The female is likely sexually aroused during this activity as well, and produces additional fluids and lubricants that promote the survival and motility of sperm, among other things.
So, it depends on many factors. If both parties are fully clothed (at least 4 layers of clothing between their respective reproductive organs) and there is a minumum of soaking through, the chances of pregnancy are correspondingly quite low. On the other hand, if only one partner is wearing just their underwear, it's essentially like there is no clothing present at all, and the relative chances go up significantly.
Safe sex practices can't be emphasized enough to young people, as education and awareness is so much better than ignorance and myths. Even aside from pregnancy, if condoms are not utilized properly to contain all the semen there is the chance of sexually-transmitted diseases, ranging from herpes and gonorrhea to AIDS. None of these require penetration to be passed along, and one might argue that the additional presence of potentially irritating fabrics could open up raw areas or cuts and enhance their transmittal.

Take home message
Now, all this being said, the chances of impregnation through clothing without direct penetration of the penis into the vagina is quite low compared to "typical" unprotected fully-penetrating intercourse, especially depending on where the female is in her fertility cycle. According to this study, a woman's most fertile day is two days before ovulation (as had been postulated before), and the chances of pregnancy on that day are about 25% (assuming penetrating intercourse). Overall, the chance of pregnancy throughout the month is about 5%.
I don't have any hard numbers on the pregnancy chances when one or both partners have at least some clothing on, as obviously it will vary greatly depending on who is wearing what, the volume of ejaculate, contact time after ejaculation, etc. Just for fun, let's assume it's 100 times lower. That means the chances of impregnation two days pre-ovulation would be 0.25%, or 1 in 400. While rather low, this is still a non-zero chance.
Condoms are about 98% effective if used properly during penetrative vaginal intercourse. Various other birth control methods such as contraceptive pills, intrauterine devices, implants and injections are quoted as being 99% effective on their own, although they do not protect against sexually transmitted diseases. I'm certainly not one for preaching abstinence, but done properly it should be 100% effective. Ultimately, it is up to both partners to decide what their risk tolerances are, together. It is much better to seriously talk about it beforehand than to be panicked and unsure afterwards.

Hopefully this addresses your concerns, please leave comments if you have additional questions.

P.S.: I am gathering all this information in order to write a few articles, to make more teens aware of the risks. Now we know that it is certainly possible by statistics and probabilities. But realistically, considering you know all the technical information about semen and sperm. Is it realistically possible? What kind of advice would you give teens whom this way of sexual interaction is their only option?

@TheNotMe after washing clothes with detergent they are generally rinsed in clean water, so the amount of "chemicals" left over should be relatively minimal. Some sperm may die, but how much of a chance do you want to take? Your best option is to wear a condom, which, when worn properly, retains the semen in the tip. It'll prevent your pants from getting soaked, make clean-up a lot easier, and give you much greater peace of mind.

@TheNotMe in regards to your second comment, yes, I think getting pregnant via "dry humping" is realistically possible. It's not very likely, as compared to unprotected vaginal intercourse, but it is definitely possible. However, like I said in my previous comment, condom use will significantly reduce the risk.

@caseyr547 could you at least explain why this is a bad answer? Comparing an answer based on scientific and medical facts to a TV show is not an answer.

@caseyr547 The point of my answer is that it is realistic. The overall likelihood is low, just as the chances of getting pregnant during any one typical vaginal sex session are, but there is a nonzero chance that it could happen, and there are several factors that affect that, as I described. I'm trying to stress that if you are going to engage in this behavior, then you need to protect yourself as much as possible. I'm also trying to dispel myths. The fewer unwanted teen pregnancies in this world, the better, and the fewer STDs the better. Calling this a bad answer is counterproductive.

It seems like it would be simple experiment to put sperm one side of a cloth barrier of a petri dish and count sperm that appeared on the other side. I'm not familiar enough with the spermology literature to know if it's been done.

Matt, It likely is a bad answer. Take a look at this WebMD blog post. http://blogs.webmd.com/womens-health/2010/01/urban-or-suburban-legends-about-sex.html from a factual perspective about pregnancy risk.

I do not think it is a bad answer from the perspective of always practicing safer sex and for people to use barrier protection at all times, to know their STD status, and only to not use protection when he purpose is to conceive and both partners have been cleared by their doctors as health, or are informed of the risks they are taking.

I've edited the answer to add some more information as well as some verified and off-the-cuff numbers, as well as discussed family planning in greater detail.

It is effectively impossible to get pregnant by dry-humping because the conditions that would have to be met for sperm to pass through multiple layers of clothes, survive on skin, find the vaginal opening, survive in the vaginal environment and finally impregnate an egg are simply unrealistic.
The barrier of clothing that we can assume present during 'dry humping' is significant. Semen begins to die as soon as it begins to dry out and any clothes you're wearing are likely to draw water away from the sperm cells through adhesion of water to the fabric. One layer is absolutely not "like there is no clothing present at all".
Assuming some sperm cells made it through all that and onto skin, their motion isn't directed towards the vaginal opening, so a sizable fraction will be literally lost at that step. Skin is also a toxic environment on its own, so these improbable sperm have a very limited time to find their way.
That last battle buddy team of sperm has very little chance of surviving the vaginal environment. A lot of sperm need to enter the vaginal environment together to ensure that just a few survive.
As far as dry humping is concerned, there's no realistic reason to worry about pregnancy.


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How does DNA damage cause ageing in yeast?
As I understand it, in yeast ageing there is daughter cell and mother cell. The daughter cell is has newly "fresh" DNA and mother cell dies after some counts of replication.
What happens to the accumulated DNA damage in the yeast mother cell?
One of theory of human ageing is accumulation of damage in nuclear DNA. The daughter yeast cell is clone of mother, and has same DNA. What happens with this damage?
Edit to simplify: Why is the DNA damage not transferred at all to the daughter cell? The repair mechanism in humans is evidently not perfect, because DNA damage is one of major ageing theories. So if we die from this, how do yeast get around the detrimental affects of DNA damage that cause ageing in humans?

I can tell there is a good question here somewhere, but its hard to figure out exactly what you are asking. Are you asking if the DNA damage is transferred to the daughter cell? If you edit to clear up the question you'll probably get a good answer. Currently it sounds like you want to know about DNA damage repair.

I am asking about why there is no DNA damage transfer at all, to daughter cell. I wrote about the theory of damage in aging, so it couldn't be in any way question about repair - because if there was good repair - it wouldn't be in aging theory. I edited the question.

Unfortunately it is becoming less and less clear what you want to know. There are some assumptions your have made that are wrong compounded by difficult grammar. Furthermore ageing is a wildly understudied area of research. DNA damage is a very complex and broad field with a lot of case studies, science, and history behind it. Specifically: "Aging in yeast (and other eukaryotic) and DNA damage" is a massive topic. It sounds like you want to know everything there is to know about it, which is not suitable for this forum and the question could get closed after the bounty ends.

I have made an edit, feel free to roll back, but the grammar at least is much clearer, maybe someone will be able to grapple the question now.

Thank you Good Gravy. I just restore back the title, because I am asking about DNA only and not about all the aging process.

It is good practice to use a question rather than a statement title (only on these forums).

Perhaps you are confusing mutation caused ageing with DNA damage repair caused ageing?

I used only the world damage. No meter what damage. Some damage to DNA that leads to cell aging (loss of some activity) and death.

This is a massive question with a few key misunderstandings of the terminology, which to be fair is complicated in the field of ageing. OP kept moving the goal posts of what the question was (as can be seen in the comments for both answers), and I doubt any answer will be good enough.

In eukaryotic cells there is no difference between a mother and a daughter cell - the later is an exact copy of the mother cell. This is true for yeasts as well for example for human cells. The only thing that happens over time is that the telomeres at the end of the chromosomes get shorter (unless the cell has an active telomerase which most cells doesn't) and it reaches the Hayflick limit where every further division will lead to a shortage of coding chromosmal regions and thus cause problems. If cells do not acquire any other chromosomal damage and have enough ressources, this would be the limit for their lifetime.
Of course there are DNA damages occuring over time. Most of them are either repaired by the highly efficient DNA damage repair system of eukaryotic cells, which consists of different checkpoints during the cell cycle. These checkpoints are located at transition between the different  phases of the cell cycle. If a DNA damage is identified, the cell cycle is stopped to enable a DNA damage repair by special proteins and to prevent that damaged cells undergo mitosis (here the G2-M checkpoint is important). This works schematically like in this figure (from the Wikipedia article on DNA repair):

If the DNA damage cannot be resolved, cells will either go into senescence (basically go into a permanent dormant state) or undergo apoptosis. If there are damages which are (for whatever reasons) are either not spotted or occur during the repair of DNA double strand breaks by non-homologous end joining, these are then replicated and inherited by further generations. Unless these errors occur during the replication process mother and daughter cells are genetically identical.
So eukaryotic cells acquire DNA damage over time (one of the reasons why late pregnancies pose a greater risk than early), but we are different from yeast in one point: Yeast has an active telomerase, which is not active in most of our cells (mainly except in stem cells). If the cells collect too much chromosmal damages than they will die.
The references listed below go deeper into the topic and are interesting to read.
References:

Negative regulation of yeast telomerase activity through an
interaction with an upstream region of the DNA primer
Cell cycle control in the kidney.
The evolution of diverse biological responses to DNA damage:
insights from yeast and p53
DNA damage and decisions: CtIP coordinates DNA repair and cell cycle
checkpoints
Cellular Responses to DNA Damage: One Signal, Multiple Choices

Thank you Chris. But, like I wrote, one one the main theories of aging is DNA damage. So how is that? If the mechanism is so good, that keeping DNA of yeast fine for millions of years, why is in human its cause aging?

@Barbos you'll want to keep in mind the generation time of a yeast cell, vs. the generation time of a human being. The exact mechanisms or processes that are damaged and cause aging are under investigation. What you'll also want to consider is that yeasts and other multicellular eukaryotes have linear chromosomes that shorten with each replication at the telomere, and may become as above: cancerous, apoptotic or senescent. Check out the NIH website for aging.

I also figure it useful to add that senescent cells secrete cytokines, ECM hydrolases etc. to aid in their timely removal by the immune system. If there's a declining immune system with age, I'd assume the ability to remove senescent cells would decrease. Of course, the regular secretion of hydrolases and inflammatory compounds will produce it's own array of damage that may lead to aging.

@kendall - no, it's not the answer. Cancer? Telomere? Declining immune system with age? It is not what I am asking about. And about "generation time" - you have some source that says that because of this, yeast cells have so much less DNA damage than human? There is cells in mammals that divide and die faster that some eukaryote organisms.

Also, what the connection with generation time? This DNA lives, no matter in old cell or in new, daughter cell. It's same DNA that influenced by environment.

The mechanism is really good - humans only generate only about 30 new mutations in their gametes per generation (I can look up the paper which makes this estimation if this is of interest for you). This is an incredible small number...this happens because of damages that cannot be repaired correctly or where the wrong strand is corrected.

Why the downvote? Can you explain whats wrong? I can only work on the answer when I know the criticism.

Because it's really not what I asked, I know about this mechanisms (but you will get the bounty - thank you for answers anyway), There are really few central aging theories (3 main), one of them is damage in DNA. (not only mutations). Also there is damage in mitochondrial DNA. (Radiation, radicals, environment and more) So this mechanisms isn't perfect but yeast need to have just perfect system... Much more stronger than ours. Because if we have damaged DNA in cell, cell die - we live. If yeast have damage - he die.

@Barbos I have edited the question now - does it answer your question better? If not, please let me know which parts are still unclear.

@Chris, thank you, but now its worse - because your first paragraph is fully wrong. There is difference between mother and daughter cell - there is asymmetric division in yeast, also there is indication that bacteria has same thing. But it doesn't meter for my question. Also it is fully wrong to say that all what happens is telomeres shorting, there IS accumulating DNA damage, this bring cancer and aging (the last is theoretical). So human die from this, but yeast no. Why?

Most of our cells are not developing into cancer cells - otherwise we all would die from it. Assymetric cells division leads to differently sized cells, but the genetic material will be the same. There are indeed some indications that this is different in prokaryotic cells, where the damage accumulates in one cell. This article is interesting in this context.

No. No. That where my question coming from. The asymmetric division not lead to same cell! Because the cell of mother yeast AGING. And when we talking about aging, one of theories is accumulating DNA damage.

Then you should edit your question again to make clear what you really want.

All are in the question.  "Why there is no DNA damage transfer at all, to daughter cell?"

Your assumption is wrong - there a transfer of DNA damages to daughter cells. It's rare, though.

If the  transfer of DNA damages is rare - why is it one of major aging theories? I just say the same things again and aging ...

It was my understanding that it was unclear whether the shortening telomerase was a cause or an effect of ageing. Is there evidence that shows cause?

Background to the different theories of ageing.
This video, from a senior lecturer at the University of Liverpool who specialises in ageing, discusses the theories of ageing. He touches on the DNA damage theory.
DNA damage theory of ageing.
Note that when talking about DNA damage theory, we are specifically talking about damage to the process of cell renewal by DNA damage repair mechanisms in stem cells.
Mutation ageing is not the same as DNA damage causing ageing and cannot really cause ageing in yeast. The idea that cells acquire damage over time due to mutated DNA is fundamentally different to the DNA damage theory of ageing. The mechanisms that lead to DNA damage are covered very well in @Chris' answer.
The suggested systemic effect that DNA damage has in the human body causes an inability to renew cells due to a lack of viable stem cells. This contributes to the process of ageing in the organism.
In yeast, this stem cell depletion process does not happen (they are single cellular mostly). In the comments it appears that you are actually talking about mutation based ageing in your original question. Mutations are passed to daughter cells. But these daughter cells don't appear to age or to die quicker (If the parental cell is 5 days old, the daughter cell does not appear to be 5 days old). This is the fundamental reason why this form of ageing remains less studied - it doesn't really make sense that general mutations cause ageing.
Summary
To directly answer the question: "How does DNA damage cause ageing in yeast?"
The question doesn't quite capture the whole picture and confuses DNA damage theory of animal ageing with general DNA damage at a cellular level.
There are many theories of ageing. Nobody knows which ones have more or less influence on ageing. Yeast is a good model for some kinds of age theory modelling, but perhaps not in the case of DNA damage based ageing. Although they experience DNA damage in the form of mutation, this doesn't cause ageing in the same way that DNA damage might cause ageing in humans because they are single celled organisms, and don't experience the same inter-tissue relationships that more complex organisms have.

Edits
This answer has been changed extensively since its first draft based on additional questions and queries from the OP in the comments. I decided to keep some important points that were raised and dismissed.

Why there is no DNA damage transfer at all, to daughter cell?

DNA damage can occur and is transferred to the daughter cell. Damage is very rare though.

So how yeast survive? Human stem cells aging and die, or get cancer. But yeast no. Human start from one cell. And die. Yeast start from one cell and live forever (dividing again and again)

Edit After Comments:
Single cell
In yeast there are no inter-tissue systems. Mutated damage is simply passed on if the cell is viable. Also the assumption that they live forever isn't entirely accurate. But the DNA is passed on in its mutated or damaged form.
Multi cell
DNA damage based ageing is a big problem for animals. (Dolle et al 2013) Showed that DNA damage to a single repair pathway causes accelerated ageing, (but note that there was not an increase in mutation during this ageing).

but you talking about cancer, it's not so good example, my mistake.  But in humans aging NOT like cancer - it occur in ALL the body and all the cells. So in all cells there are some DNA damage.

Another edit: You were right to talk about cancer in this context. The DNA damage theory of ageing is that small changes (damage) in our DNA accumulate over time and damage cell types by damaging various DNA repair pathways.
Damage accumulates and over time less stem cells for renewal are viable and cellular repair of other damaged cells slows down.
Also this same fundamental principle of mutation damage happening over time can lead to mutations that switch off cell control mechanisms and lead to cancer. Although these these mutations do not increase in rate with age (Hill et al., 2005).
For example the naked mole rat lives 10 times that of comparable species (less ageing) and have not been observed to naturally acquire cancer (less cancer). The theory implies that the two things are quite linked because of the way DNA changes, but not that specifically mutation is a cause or result of ageing.

I talking more about aging. Because there is aging in yeast. And one of aging theories for human - accumulating DNA damage. So what Chris writing is that it's really rare.

**Stem cells are damaged. ** I'm no longer entirely sure of what you mean by ageing in yeast. Yeast aren't reliant on a limited number of stem cells for cellular renewal, they don't age in the way you might be thinking. They simply proliferate the mutated cell type. There is no impact to a larger organism like in human ageing.
DNA damage. Yeast is a very helpful organism for understanding the underlying biochemistry and genetics of ageing, not the overall ageing systems. These are two different fields of study. It is unclear which you are talking about at this point.

Also there is aging in places where no stem cells - like brain - no renew of cells, just existing cells age, damaged, die, and not replaced.

Dolle 2006 found that spontaneous DNA damage in relation to age happened in the liver but not the brain.

Also you telling us that there is no cancer.

No & No. The damage is rare, but it does occur so much that cancers may develop naturally in animals and may cause ageing over time. Remember cancer is a huge field of different diseases.

So how yeast survive? Human stem cells aging and die, or get cancer. But yeast no. Human start from one cell. And die. Yeast start from one cell and live forever (dividing again and again)

thank you for edition, but you talking about cancer, it's not so good example, my mistake. Sure there is no cancer in single cells. I talking more about aging. Because there is aging in yeast. And one of aging theories for human - accumulating DNA damage. So what Cris writing is that it's really rare. But in humans aging NOT like cancer - it occur in ALL the body and all the cells. So in all cells there are some DNA damage.

First of all, thank you! About yeast aging and "limited number of..". The yeast has limited number of divisions, mother cell die after some count of them. I am not asking why, I just taking ONE of the theories of human aging (accumulating DNA damage) and asking, if the same theory is right to Yeast, how is it possible that daughter get no damaged DNA, when mother die because it (one of theories).

About the main part "don't accumulate as much damage" - but the DNA lives 'forever'. It's the same DNA - what meter if it in old cell or in new? One mutation  transferred to daughter. Accumulate new damage (already 2), transfer to new daughter, another damage (already 3) ....

In my answer I explain that the DNA damage theory of ageing is not directly applicable to yeast as DNA damage theory of ageing affects stem cells and stops repair of tissues, so the whole massive 37 trillion cell human organism suffers. In yeast, the DNA damage doesn't have this affect and 'ageing' in that context does not occur despite there being DNA damage passed down the lineage of cells. What do you mean "DNA lives forever"?

I don't agree about  repair of tissues. DNA damage leads to problems in cell that damage occurs in. Doesn't meter if it steam or not. Damaged DNA can't make some protein or do bad one. So it's directly  applicable to yeast - in my opinion. Damaged DNA, not producing of important proteins - death.

About DNA lives forever. You say that there is no time to damage to accumulate because short life. But the DNA it self doesn't have short life. DNA (lets say one of single string) lives forever. And the second string is just a cope. Lets say we have a small damage in mother (G instead of C) and it doesn't influence. It pass to all the daughters. One of daughters take another damage (one A to T) so now we have already 2 damages in DNA. And it's go forward accumulating more and more. It doesn't meter that the initial cell already dead.

Unfortunately, it doesn't matter what your opinion is; The most current form of the theory of DNA damage based human ageing is that long lived stem cell stocks are depleted. For regular DNA damage you are right. It happens in yeast and humans. But ageing in humans is a more complex systemic and generally predictable process rather than random changes to random proteins. And always remember, this is one of many theories of human ageing and it possible many of those theories are right.

Damage in stem cell = stem cell not working. Same damage in yeast cell = yeast cell don't work. Also there is aging in places where no stem cells - like brain - no renew of cells, just existing cells age, damaged, die, and not replaced. Aging of stem cells cause by DNA damage (one of the causes) so in the same way it cause damage to yeasts. I talking only about DNA damage and not other theories. The DNA damage have some part in it - that is the theory. So in the same way it need to affect yeast too.

Damage in stem cell = stem cell not working = no cell renewal = ageing? The brain does not age quicker when DNA damage is increased (see modified answer, Doll et al 2013). Fundamentally you are misunderstanding that yeast and humans propagate in different ways. Another misunderstanding is that this form of ageing does not apply to yeast. But I hope I have helped a little. If you have any more questions or thoughts, feel free to move this to the discussion.

Thank you, Good Gravy. I will dive dipper in this topic. But about the brain, for example, in wiki "Accumulation of DNA damage with age in brain has been reported during the period 1971 to the present in at least 29 studies" (http://en.wikipedia.org/wiki/DNA_damage_theory_of_aging) there is a lot of studies that talking about accumulating damage in all body cells (not just stem). "The source of the DNA damages ... appears to be reactive oxygen species, produced as byproducts of normal cellular metabolism." Yeast produce same  reactive oxygen. Wiki talking about damage to single, not stem, cell

This is why there are many theories; each has evidence for and against it. Nobody know which contributes the most to ageing. Here we are discussing DNA damage only. The mutation theory is different. Perhaps open another question?

What meter how many theories is? Also I didn't talked which one more important.. I getting answer to questions that I didn't asked. I telling again and again. DNA damage is one of the theories of aging of single cell in human body (not only stem, regular cells). Because of all the DNA damage (mutation,oxidation,mistakes, doesn't meter) cell lose the function and die. Why it isn't happens in yeast? All your answers very interesting -but that not what I am asking for. There is similarity between yeast cell and human cell. They both get DNA damage, for example from reactive oxygen from metabolism

"This is why there are many theories; each has evidence for and against it" How is that connected to my comment? I wrote just about one thing - DNA damage.


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In a typical model ecosystem, what might the percentage of plants be to top predators and everything inbetween?
I'm not sure if this will be a simple question that is almost a natural law for an ecologist, or a complex serious of assumptions.
I vaguely remember from school that only 10% of the energy is converted to biomass at each 'level up' however I have never seen any academic support of this. Lets say we have a fairly representative model ecosystem. In a pyramid of biomass, what percentage of biomass would I expect to see at each level (top predator, primary predator, herbivores, plant mass)?
An additional part I would like to know is does this ever correlate to the ecosystem of any given tier. i.e typically 5 predators will be found in the same area as 20 herbivores rather than 10% of predator biomass for 100% of prey.
There are plenty of diagrams available on google, but I have yet to see anything that looks credible. Any citations to academic sources would be greatly appreciated.

The percentage of biomass at each stage will vary tremendously, based on the following factors:
1: Relative turnover rate of the biomass. When biomass turnover is very high (for example in plankton and whales), it is possible for whale biomass to exceed that of the plankton, even through the whales feed on plankton. Therefore, it is better to use a pyramid of energy, where the total energy flux through a specific trophic level is used. See the article here for more detail.

Just as with the inverted pyramid of numbers, in some rare exceptions, there could be an inverted pyramid of biomass, where the biomass of the lower trophic level is less than the biomass of the next higher trophic level. The oceans are such an exception because at any point in time the total amount of biomass in microscopic algae is small. Thus a pyramid of biomass for the oceans can appear inverted (see image part b). You should now ask "how can that be?" If the amount of energy in biomass at one level sets the limit of energy in biomass at the next level, as was the case with the hares and foxes, how can you have less energy at the lower trophic level? This is a good question, and can be answered by considering, as we discussed in the last lecture, the all important aspect of "time". Even though the biomass may be small, the RATE at which new biomass is produced may be very large. Thus over time it is the amount of new biomass that is produced, from whatever the standing stock of biomass might be, that is important for the next trophic level.

2: Biomass conversation rate in each trophic stage. For example, the article on entomophagy cites a number of papers that insects convert vegetation to biomass approximately 10 times more efficiently than cattle. A population of humans that fed on cattle would have a different biomass (and energy) pyramid than a population of humans that fed on locusts, for example.


text:
Why does uniprot sometimes not label single-pass transmembrane proteins as "anchors"?
Currently, section 3a) of unitprot TRANSMEM reference page divides single-pass transmembrane proteins into 4 types: I, II, III, IV. I is not explicitly labelled as an "anchor" whereas the others are. What criteria need to be made for a single-pass protein not to be classed as an anchor?

A membrane anchor is close to the end (N-terminus or C-terminus) of a protein. For "Single-pass type I membrane proteins" the transmembrane region is not necessarily close to N- or C-terminus, which is why single-pass type I membrane domain are not labeled as anchors.
Instead, relevant entries usually have a signal peptide annotated.
Note that we have replaced the example for single-pass type I membrane protein by http://www.uniprot.org/uniprot/P14778#subcellular_location which is more relevant (the modified version of the documentation will be available with release 2016_01).


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Ostium: insects circulatory system

What is this? Is this a part of the tubular heart? Does it pump hymolymph? Does it have ostium?

I will alter this answer in response to the poster's comments.
Looking at:
https://genent.cals.ncsu.edu/bug-bytes/circulatory-system/
The diagram doesn't show the digestive system - so no anus.
I see that there is expected to be an ostium (hole) near the end of the heart.
Think about where in the heart the many valves are located, then look at the segments of the abdomen and work out what happens with the heart when the abdomen extends or contracts, which you can see in bees.
What is more interesting in all the diagrams is the decision about whether the heart pumps just to the head, or also through pipes to the ventral region.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Skeletal muscle has got many many peripheral nuclei. What does "peripheral" mean here?

Cardiac muscle has got a central nucleus similar to smooth muscle, but skeletal muscle you may recall has got many many peripheral nuclei.

What does "peripheral" mean here?

Maybe you can add the source of the citation to have a clearer context

@havefun More info added

Skeletal muscle nucleui are peripheral located because they have a large muscle tone compared to the cardiac and smooth muscles.

'Peripheral' in this context refers to the position of the nuclei within the skeletal muscle cell.  They are in the periphery (outer part) of the cell body rather than central as in most cell types.  More specifically, they are "subsarcolemmal", i.e. just under the sarcolemma, the cell membrane of the muscle fiber cell (source):

(Image from Wikipedia)
The many nuclei of a skeletal muscle cell are spaced out along the length of the cell (source 1, source 2).


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What makes the electrical charge inside the neuron more positive at the end of action potential and returns it to resting potential?
When a neuron's stimulated by something, electric potential difference changes immediately and inside of the neuron, becomes more potentially positive than the outside of it.
I've read that sodium-pottasiom pump returns membrane potential back to its resting potential at the end of action potential's process.
How sodium-pottasiom pump returns membrane potential back to its resting potential and makes inside of the neuron more potentially possitive when three sodium ions are transported to the out of the cell and just two potassiom ions are transported back into the cell?
I mean, in this condition, it is expected that inside of the cell is gonna be more potentially negative, not more positive.
(Sodium-pottasiom pump ➡ puts 3 Na+ outside - brings 2 K+ inside ➡ 1 negative charge inside...!??)

The issue is the permeability of the membrane to Potassium and how membrane potential is created in the first place. The resting membrane potential of the neuron is very close to the equilibrium potential of Potassium. Large fixed anions (proteins) in the cytosol are represented in the image below by [An-]:

If Potassium and cytosolic proteins were the only thing inside the cell and the outside were water (ignoring osmotic effects), then in Figure 1 there is an outward K+ concentration gradient.
In Figure 2, we allow the membrane to become permeable to Potassium (as it is in the cell). The Potassium begins to leave [green arrow], but as it does, it begins to create a charge separation that sets up a negative voltage in the cell that pulls the Potassium cation back in [red arrow].
In Figure 3, we see that enough K+ has left the cell to the point that the membrane potential has grown negative enough that the rates of K+ leaving and entering are equal, so no net change in K+ concentration occurs. This is the definition of chemical equilibrium, and so we call this voltage the equilibrium potential of this single-ion system (~-80mV for biologic concentrations of K+).

We could do a similar experiment with Na+ starting high outside in Figure 1, with the arrows reversed, and the equilibrium potential of the Sodium-only system would be ~+60mV.
So, if a real cell has both K+ and Na+ concentration gradients in opposite directions, why don't they just cancel each other out? Why is the resting membrane potential negative, and in fact, much closer to the equilibrium potential for Potassium alone? The answer is: permeability. Imagine if you had Figure 1 again, with [K+] high inside, and [Na+] high outside, as it is in the cell, but in Figure 2 you ONLY made the membrane permeable to K+. Would the Na+ gradient change at all? No, because there would be no pathway for it to move. Thus, if ALL the permeability is for K+, then K+ has all the influence on the membrane potential. If both are equally permeable, it would be their average (-10 mV, or about neutral).
However, the permeability for K+ AT REST is about 20 times the permeability for Na+, so we'd expect the cell's resting potential to be 1/20th of the 140mV "distance" between the equilibrium potentials for K+-only and Na+-only systems, or: -80mV + 1/20(140mV) = -73mV. The fact that it's not exactly -73mV is explained by the existence of a small amount of Cl- and other ion permeability. But, in essence, Potassium determines the resting potential, with a little offset due to sodium permeability.
Now that you understand that, understanding the action potential graph should be easy:

Rising Phase: major increase in Na+ permeability, voltage rises almost to the equilibrium potential of Sodium.
Falling Phase/Undershoot: Na+ permeability shuts down, major increase in K+ permeability, voltage drops back down to equilibrium potential of K+.
Restoration: K+ permeability drops back to normal (not completely shut down), and the Na+/K+ pump just restores the concentration gradients that allow the resting potential in the first place.

So, really, your initial confusion about the electrical work done by the Na+/K+ pump existed because you didn't take it in context with the permeability. Yes, the pump by itself makes the voltage more negative, but some of the potassium it stuffs back into the cell immediately turns around and leaks right back out until it's 95% of the way to its own equilibrium point again, as determined by the membrane permeability.

So do you mean that after action potential some K+ channels are actually open and they allow K+ ions to come inside the neuron, and it is, therefore, returned to resting potential, and the neuron becomes more potentially positive in a way that it neutralizes the activity of Na+/K+ pump?

Yes, sort of. Remember: Without a concentration gradient in the first place, there would never be an electrical gradient. There are two transport proteins which are always on/open, and their actions combined make the resting membrane potential: the Na+/K+ ATPase and ungated K+channels. They perform their function even throughout the duration of the AP. [1/2 - trimmed for length, see next comment]

Neurons and striated muscle have other K+ channels that only open when the voltage gets to about ~0mV, near the end of the rising phase of the AP, and are thus voltage-gated. Their closure is what causes the change in slope during the overshoot phase. Like any other chemical process, the membrane potential then returns asymptotically to what the steady state is when all the voltage-gated channels are closed.[2/2]

But all in all I cannot find out this sentence I've read in lots of books: "Sodium-pottasiom pump returns membrane potential back to its resting potential at the end of action potential's process." It is K+ channels  that does this action NOT Sodium-pottasiom pump, I suppose!

No. As I said in the above comment, It is BOTH the Na/K pump and the non-gated K+ channels that create the steady state (resting) membrane potential. Think of the AP as a disturbance, like a wave in a calm pond. Gravity is what made the water flat before the wave, and gravity will return it to the calm flat state. Gravity didn't stop pulling down on the water's surface while the disturbance occurred. Similarly, the Na/K pump creates the flat line in the above graph, keep trying to create it while the EPSP and voltage-gated disturbance happens, and they are responsible for re-flattening it.

What do we exactly call those special K+ channels?

The "always-on" channels aren't the special ones. They are ubiquitous in the body. The voltage-gated ones are the special ones. They only exists in excitable cells. For a better list of potassium channel types, check Wikipedia

The undershoot or afterhyperpolarization arises due to the increased K+ conductance at the end of the action potential. This is because K+ channels where open during depolarization and it takes some time to close again. Also Na+ channels are inactivated and getting out of this inactivated state also takes time.
So why the potential rises again after this undershoot?
This is because K+ channels start closing and thus the membrane permeability for K+ decreases. This makes the membrane potential increase, until it gets back to the resting potential.
The role of the pump is to maintain the ionic gradients of the neuron helping to maintain this resting potential.


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Prostate, seminal vesicles or testis which one is bigger(by volume and size)?
I can't understand this by looking at these photos, especially the last picture makes me more doubtful.
Do you know which of them is the biggest one by volume?

Another question is, what is the biggest organ in the male reproductive system? (Note that the bladder is not a part of it.)

Why does it matter?

@Bryan-Krause Comparing the size of male reproductive system organs

That doesn't answer the question of why it matters.

@BryanKrause  Be sure that I don't want to know this just to satisfy my curiosity, I faced with it in my multiple choice test. I don’t think it matters much what you study anyway.

I'd note that the images you've examined are representations, not specimens. Generally, don't expect everything to be to scale. I'd suggest Rohan's Color Atlas of Anatomy if you want actual specimens. There is a plate there that should help you.

@BryanKrause the relative size of anatomical structures is a reasonable question in and of itself. It's useful if, for example, you want to identify them. OP, you've asked two questions: which is bigger, the prostate or the seminal vesicle, and what's the biggest organ. You could improve this question by defining your terms (bigger how? by volume?) and by limiting it to a single question.

The average seminal vesicle length was 31±10.3mm and its average volume 7.1±5.2cc. That is verified by another source which states 6-10mm in controls.
The average prostate volume ranges from 20 to 40cc from ages 30  to 80, 3-2-3cm for younger males 5-4-5 for older ones.


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The organisms of the same species with a different number of chromosomes
I am looking for some specific creatures. The organisms of the same species that have different chromosome numbers. Just like male grasshopper (23 chromosomes) and female grasshopper (24 chromosomes).
(Please disregard any disorders such as Trisomy 21 in humans or other disorders in other organisms.)

Well this applies to many, many species of insects.  While a few different sex determination systems are at use in insects, including xy (fruitflies), xo (grasshoppers), and zygotism (ants), all of them other than xy involve differing chromosome numbers between males and females.  xo is the system you discuss in your question, where females have an extra x chromosome and males don't, with no equivalent to the y chromosome present.  In this case, females always have one more chromosome than males.  In zygotism, the sex determination system seen in ants, bees, and most wasps, males are haploid (possessing only one copy of each chromosome) and females are diploid (possessing 2).  This means that females have twice as many chromosomes as males.  Interestingly, it is this odd form of sex determination that appears to have driven the evolution of these species into eusocial insects.  If two sister bees share the same mother and father, they each got half of their mother's DNA and all of their fathers DNA, since he is haploid.  That means that they share 50% of DNA in common with their mother and any children they might produce but 75% in common with eachother.  Due to this genetic eccentricity, a bee gets more of her DNA out there by protecting and helping her mother push out more sisters than she would by having children of her own.
Outside of the insect world, we have other mechanisms for inducing chromosomal differences that are not related to sex determination.  You mentioned trisomy but this is really just the tip of the iceberg.  Polyploidy, mutations resulting in more than 2 copies of one or more chromosomes, and anuploidy, the deletion of one or more chromosomes, are very rare in humans, with trisomy 21 being the only really publicly well known example, but common in some other species.  Ferns and other simple plants regularly duplicate all of their chromosomes, resulting in triploid and quadroploid offspring that are still viable and able to produce children of their own.  Mice are also very susceptible to this type of mutation, to the point that there are currently 97 separate populations of the common house mouse characterized by various chromosomal eccentricities.  Here is a rather interesting study on this tendency in the common house mouse.
Chromosomal variation in the house mouse

haplodiploidy is the term for organisms in which one sex has half the chromosomes as the other sex.

Well. Can we come to this conclusion? "In normal circumstances (by ignoring chromosomal abnormalities), organisms of the same species with the same sex must have the same number of chromosomes."


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Flatworms sexual reproduction; one must be the mother and the other the father?
I watched this.
I wonder if both of these flatworms ever end up pregnant.
Earthworms are simultaneous hermaphrodites, meaning worms have both male and female reproductive organs, just like flatworms. During sexual intercourse among earthworms, both sets of sex organs are used by both worms. If all goes well, the eggs of both of the mates become fertilized. Can this occur in flatworms?
Or in flatworms, one must be the mother and the other the father?


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Do all monarch caterpillars have two pairs of needle-shaped protrusions(or they can have three pairs)?
I found this here:

Is this a monarch caterpillar?
Do all monarch caterpillars have two pairs of needle-shaped protrusions?

Just a guess, but it may be species-dependent on whether they have 2 or 3 pairs of protrusions/antennae. Your first image is of Danaus chrysippus, while your lower image is of two other species.

@MattDMo Danaus chrysippus and Danaus gilippus caterpillars are very similar. Quite difficult to distinguish.


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Does Krebs cycle occur in fast glycolytic muscle fibres?
They have mitochondria. So they can have aerobic respiration. (?)
Does Krebs cycle occur in their mitochondria?

Could you please clarify. What do you mean by an “effective” enzyme, and inhibited under what circumstances. The enzymes of the Krebs Tricarboxylic Acid cycle are located in the mitochondria, so their total activity in a cell will obviously depend on the number of mitochondria. But surely that isn’t your question.

@David Our examiner used this term "effective" just the way I put it in the quesion. So effective, how? I don't know either.
But I think we should consider all enzymes that somehow take part in Krebs cycle.
So as you said I think we should consider the enzymes that are located in the mitochondria.
Does aerobic respiration and Krebs cycle occur in white muscle cells?
If they do, then these enzymes are active in mitochondria of white muscles as well as red muscles, but the number of these effective enzymes are fewer in white muscle cells.

The point of mitochondria is aerobic respiration using the TCA cycle, the electron transport chain, and generation of ATP by oxidative phosphorylation. Different muscles types in different species vary in the extent their action can be sustained by a supply of oxygen, so they vary in their content of mitochondria. Although for teaching purposes it is useful to contrast extreme fast-twitch and slow-twitch muscles, there is no requirement for a muscle to be completely anaerobic. Those mitochondria that are present can use that oxygen (and substrates) that are available.


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"Bacteria don't have membrane-bound organelles." Are sulfur bacteria or Cyanobacteria exceptions?
Can bacteria have membrane-bound organelles?
I read this many textbooks:

Bacteria cells are simple cells that do not contain a nucleus or other membrane-bound organelles. However, they do contain other cellular structures that aid with their life processes.

Or here:

Prokaryotic cells (Figure below) are usually smaller and simpler than eukaryotic cells. They do not have a nucleus or other membrane-bound organelles. In prokaryotic cells, the DNA, or genetic material, forms a single large circle that coils up on itself

Are sulfur bacteria or Cyanobacteria exceptions?
Sulfur bacteria because they have big vacuoles. (Vacuoles do have membrane, don't they? Or maybe something is different about prokaryotic vacuoles that I don't know?)

A vacuole is a membrane-bound organelle which is present in plant and fungal cells and some protist, animal and bacterial cells. (1)

And
Cyanobacteria because they have gas vesicles. (These vesicles are membranous, aren't they?)

(1): Schulz-Vogt HN (2006). "Vacuoles". Inclusions in Prokaryotes. Microbiology Monographs. 1. pp. 295–298.


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Are axons of neurosecretory cells in neurohypophysis myelinated?
According to the pictures that I found in textbooks and Google here these neurons are not myelinated.
I just wanted to be sure. They are not myelinated, are they?


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The position of the macula in comparison to the blind spot
Which is located in a higher postion? Macula or blind spot?

The first image is a section of the eye. What was the plane of this section: longitudinal, transverse, or something else? Also, for the second image, what was the orientation of the camera? Are these images of the right eye or the left eye? Thinking along these lines will lead you to the answer.

@Adhish The first image is a section of the left eye and the second one is also of the left eye. Can we say that macula and blind spot are almost in the same positon or level (horizontal)


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Are humans the only mammals that are known to display homosexuality?
REQUEST: In this post I do not refer to, nor do I encourage reference to, any ethical/moral/emotional aspects of homosexuality. So please don't start an pro/anti- LGBT campaign in the comments section.

Are mammals (other than humans) known to engage in homosexual activity of any sort?
From the way I see it, homosexual activities carry no evolutionary or reproductive benefit: No offspring produced, no continuation of species...hence pointless.
Yes, I get that the "need to mate and to produce and protect offspring" is hard-wired into every (normal) mammalian brain. If I've interpreted this correctly; intercourse is a fairly energy-expensive act so if there were no immediately clear "incentive" for mammals to mate they wouldn't mate at all, hence heralding the decline and eventual extinction of a species. Nature solved this conundrum by ensuring that the brain would perceive intercourse as highly pleasurable, thereby securing the necessary "incentive" for mammals to mate.
The only "flaw" here, is that simply stimulating the genitals is sufficient enough to elicit a sensation of pleasure. So there's no real need to go through all the trouble of finding a suitable animal of the opposite sex and "do it" to feel good. A sufficiently intelligent mammal would soon figure that out; so this opens up two more possibilities: 1) Masturbation and 2) Homosexuality. (Since this post's on Homosexuality, I'm only going to deal with the latter)
So, a mammal intelligent enough to figure this out would have three options before it : 1) Heterosexual activity, 2) Masturbation, 3) Homosexual activity; the last two options being a way to bypass Nature's original intent.
So before I continue, I want to make what I mean by "homosexuality" very clear:
a) A being that displays option 1) or both 1) and 2) is heterosexual.
b) A being that displays options 1) and 3) [and maybe 2) too] is bisexual.
c) A being that displays option 3) or both 3) and 2) is homosexual.
[Just to make it explicitly clear, a homosexual will always steer clear of option 1)]
So let me just put all of that together and re-phrase my question:
Q- Are there any known instances where a (non-human) mammal consciously avoids heterosexual acts and instead prefers to engage in homosexual activity
Personally, I find this doubtful, since the existence of homosexuality (among humans) is the unintended result of Human self-consciousness/intelligence, something that other mammals apparently lack.
HOWEVER: (Considering another possible reason for homosexuality)
If occurrence of homosexual tendencies is (also) due to, say, the stochastic, faulty "hard-wiring" of the human brain due to mutation or damage to neural tissue (I'm not sure if this really is one of the reasons for homosexuality), then it would seem plausible that other mammals could also be affected by this stochastic "fault" and thereby display homosexual tendencies.

Have you looked at the wikipedia article on homosexual behaviour in animals?

@Remi No, no I haven't ._.

Sentences like the last two options being a way to bypass Nature's original intent. seems at least partially opinion based. You might want to have a look at the post How can homosexuality evolve despite natural selection?. Note also that there is no such thing as intention in nature but I suppose it was only a way of speaking)

@Remi "...I suppose it was only a way of speaking" It was ;)

Since answers will deal with homosexuality, I just want to mention that masturbation is quite natural as well, even porcupines do it. there are several hypothesis about its function with varying levels of support. Most likely several are true.

Although intuitively it would seem unlikely that there could be an evolutionary advantage to homosexuality (other than some theories regarding population control), homosexual behavior has been clearly observed in a variety of birds, monkeys and apes, lions, dolphins, lizards, insects, and plenty more.
The case of the bonobo is particularly striking in that homosexuality and bisexuality are more common than heterosexuality.  According to this Wikipedia article:

Bonobos, which have a matriarchal society, unusual among apes, are a fully bisexual species—both males and females engage in heterosexual and homosexual behavior, being noted for female–female homosexuality in particular. Roughly 60% of all bonobo sexual activity occurs between two or more females. While the homosexual bonding system in bonobos represents the highest frequency of homosexuality known in any species, homosexuality has been reported for all great apes (a group which includes humans), as well as a number of other primate species.

Although the complexity of sexuality likely points to the existence of multiple genes playing a role in sexual behavior and preference, at least one study$^1$ points to a single gene playing an important role in the sexual behavior, of female mice:

In this study, we generated mutant mice specifically lacking the FucM gene that encodes fucose mutarotase. The homo- and heterozygous mutant females exhibited deficits in sexual receptivity as demonstrated by a drop in lordosis score. Moreover, the mutants displayed masculine behaviors and preferences to female urine over male urine.

1) Male-like sexual behavior of female mouse lacking fucose mutarotase, Dongkyu Park, Dongwook Choi, Junghoon Lee, Dae-sik Lim and Chankyu Park, BMC Genetics201011:62, DOI: 10.1186/1471-2156-11-62

Regarding your first sentence: https://biology.stackexchange.com/a/7675/107

@kmm , interesting studies cited, particularly the twin study. Too bad there isn't more understood about the why of it, as in why heterosexual relatives of homosexuals are more promiscuous. Something to do with a balance of hormones maybe. Pretty complex picture. Thx for the link.

This reminded me of the rat overpopulation experiments from the 1960'sish, in a nutshell, if rats are allowed to overpopulate in a confined area, the males become stressed, violent and homosexual.

Whoa! That's something you don't hear everyday. Did the study suggest any reason for male homosexuality in this case? (I can't seem to think of any )

I can't remember any, other than as a means of displaying dominance, it has been used by armchair scientists as an example of why overpopulation leads to depravity and the "sin" of homosexuality. But mainly it's been used to guide animal welfare standards (at least in lab animals).


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Moth that resembles a leaf. What species is this?

Location: Urban area near the Western Ghats, Kerala, South India
Date: Sometime in September, 2016
Climatic Conditions: Humid, frequent rains.
Brief description:
Head isn't prominent from the dorsal view. Wings outstretched even when at rest. Antennae largely concealed under the fore wings. Also it...um...does a pretty good impression of a leaf.

It resembles Pelagodes antiquadraria, which belongs to the moth genus Pelagodes in the family Geometridae.

Image Source: FlickRiver

Not a Moth, it's a Geometrid emerald butterfly.
http://www.fnanaturesearch.org/images/stories/ns/marked/M/7002.jpg

But that picture looks quite different from the one above, especially the white lines and maybe the "feathery" edges of the wings.

Although it belongs to the family of Geometrid, its belongs to a moth genus