text:
Is it ok if I define Genes this way in Biology?
Genes are found in chromosomes and their job is to show us the traits of someone (height/hair color)
I do know that alleles specify the height of the person (Tall/Short) and their hair color(blue/green), etc. So is it correct to define Genes this way in my exam?

Not all genes have a corresponding phenotype.

Obviously, otherwise we would all look the same..xD

@OkamaKsakas Not sure what you mean by that. There could be multiple alleles for any given gene.

The term gene has been defined (by Wilhelm Johannsen) much before we even knew about the structure of DNA (by Watson and Crick). As such, a gene is typically a vaguely defined functional unit in the genome that codes for a gene product (typically a protein). Have a look at the wikipedia entry for more info.
For a given gene, you might have different variants. Such variant is called an allele. Let's consider a given phenotype such as eye color for example. There would be a gene that we could call "EyeColor" and there could have different alleles at this gene that we could call "BlueEyes", "BrownEyes", "GreenEyes", ...
Of course, in reality it is rarely that easy. A given phenotype is often the result of the interaction of alleles at several genes. Also, the environment (type of food, temperature and many other things) affect a lot the phenotype of an individual.
From your comments, it is made clear that you do not understand the interplay of the different factors that affect variance for a phenotype in a population, you have to understand the concept of heritability. You might want to read Why is a heritability coefficient not an index of how “genetic” something is?.

Genes are found in chromosomes

This sounds like a chromosome is a box containing genes which is misleading. In this regard, I like the folded shirt analogy by @terdon below in the comments.

and their job

In science, always avoid the concept of purpose, of goal, of intention. Things just happen.

is to show us

As if genes wanted to please humans. Sounds very wrong.

the traits of someone (height/hair color)

Genetic variance in population does affect phenotypic variance in the population indeed.
Answer to comment

just want a clarification on why genes are found in chromosomes isn't clear?

No, it was not clear and it still is a bit unclear (but I'll give some info below that will hopefully help). The easier for you is probably to have a look at an intro course to molecular genetics such as this one by Khan Academy for example

DNA is found in chromosomes, and large strings of DNA are genes so why?

DNA is a big molecule which contain the genetic information. It looks like that

To be more accurate the genetic information is held in the sequence of base pairs (base pairs shown on the figure). In eukaryotes (animals, plants, fungi and others but not bacteria, archea or viruses) there are several big molecules of DNA and each one is organized into a chromosome. Here is a drawing to help you visualize that

If you screen through a human genome, you will realize that the vast majority of the sequences of base pairs are not within genes. There are many other sequences such as regulatory sequences, repetitive sequences and other things. Note, also that within a gene (but again the term gene is typically poorly defined) not everything will end up coding for a protein. Only about 1.5% of the human genome directly code for a protein.
Giving you a complete answer would require writing way too much. It is much simpler to seek for further information on such introductory questions in a introductory course to molecular genetics (as the khan academy course I recommended earlier).

I just want a clarification on why genes are found in chromosomes isn't clear? DNA is found in chromosomes, and large strings of DNA are genes so why? http://prntscr.com/dsilt0

@OkamaKsakas Please see edit.

@OkamaKsakas DNA isn't found in chromosomes, it is organized into chromosomes. The chromosomes don't "contain" DNA just like a folded shirt doesn't "contain" a shirt. It is a shirt.

Do you mean that chromosomes are the DNA and if so why do we call them chromosomes? and isn't the gene the sequence of DNA? so how come..

@OkamaKsakas You should really just follow an intro course, it would save you much time.

No.  A gene is a sequence of DNA that codes for a gene product, like a protein.  An organism's phenotype is determined by all its gene products, and interactions with the environment.


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Which algorithm to find the evolutionary relation of 5 sequences?
After Multiple Sequence Alignment (MSA), data sets are produced on which models of evolution are used. I've seen in books that if there is strong similarity between the sequences then Maximum Parsimony (MP) is used, if that is low then Minimum evolution, and if there is very weak similarity then Distance based Method is used. However, all of these have their own cons.
Since character based methods are more reliable (as book), Can these methods be used even when there is low sequence similarity?
Are there any algorithm that builds the precise tree model without considering similarity of the sequences?

How do you measure sequence similarity? What book do you refer to?

Multiple sequence alignment ? D W Mount, bioinformatics sequence and genome analysis..

If you work with protein coding sequence and on the DNA level their to divergent, then it is better to use the amino acid sequence for alignment and phylogenetic reconstruction.
Better sampling can also help you, for this you can check the online databases with BLAST to find similar sequences that would fill the gap.
The problem with sequences with low sequence similarity is that it is difficult to identify homologous positions/characters and all alignment based methods rely on the assumption that the aligned positions are homologous.
Finally, there are alignment-free algorithms as well. (https://en.wikipedia.org/wiki/Alignment-free_sequence_analysis)
In general about algorithms for phylogenetics:
Nowadays, journals usually require you to run maximum likelihood (ML) analysis or Bayesian analysis. Both of these methods are referred to as model based. The most common programs used for these are RAxML (ML) and MrBayes (Bayesian). Another common software is MEGA (Molecular Evolutionary Genetics Analysis), which can run different tree building algorithms.
Usually, for quick reference maximum parsimony or neighbour-joining trees are good. For publication a maximum likelihood tree is very useful, since it returns a single best tree. While Bayesian analysis and maximum parsimony return a collection of trees.
It is also helpful different algorithms and if all return similar trees than you can be more sure about the relationships.

Can you add sources to allow users to background read on your answer? Could you tell us the benefits of the methods described in terms of the question? Of now, it seems more like a general comment than an answer

I added a bit more targeted part to the answer. I don't exactly know of reference for what I wrote in the general part. It is what I hear from colleagues and see in current publications.

source: Stack Exchange

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Anatomy of seeds (dicot and monocot)
Do all dicot seeds have endosperm? Will they be retain as they grow and what are the difference with its monocot counterpart?

You are asking a broad question. Can you please add relevant details to narrow down your question so that it is answerable in a few paragraphs (at max).

Will dicots always have endosperm?

no all dicots seeds don't retain endosperm, e.g.: Fabaceae

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Besides X. morgani praedicta, are there any species whose existence was predicted before they were discovered?
The orchid A. sesquipedale has a spur so long that at the time of its discovery, no insect was known that could pollinate it.
This led Charles Darwin to predict the existence of an undiscovered moth based on the idea that the moth and the orchid had co-evolved. That moth, X. morgani praedicta, was subsequently discovered in 1903 – a triumph for early evolutionary biology.
Has it ever happened again that a species was predicted to exist before being discovered?

I'd imagine there would be numerous examples of this. One species I can think of is Monocercomonoides sp., before the discovery of which we didn't know any examples of eukaryotes that had completely lost their mitochondria, or the derived forms of these organelles, such as hydrogenosomes and mitosomes. A prediction wasn't necessarily coined by any particular person like in your example, although there might be some papers somewhere that make such a prediction, I'm sure many people hypothesised that it was probably possible for eukaryotes to completely lose mitochondria if their iron-sulfur cluster biogenesis pathway was replaced by a cytosolic system that could fulfil the same role but we didn't know of any that had.

See paper: http://dx.doi.org/10.1016/j.cub.2016.03.053


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Why are peas in mendelian genetics different?
In mendelian experiment, yellow seeds were seen to be dominant over green seeds. The peas I've seen are generally green and not yellow. Did he use a different variety of pea plant ?
The other trait that was seen was white or grey seed coat where grey is dominant over white.
Why are these results not consistent with the peas found in pea pods ?

If I had to guess, they were varieties of pea plants that we aren't accustomed to dealing with.

The yellow colour of pea seeds is a rare trait and is found in many parts of the world ,China and Fiji islands for example. It's not usually found in Indian market though.(Wikipedia)

@SanjuktaGhosh I think that's what OP is looking for, and you should submit it as an answer!

@Gaurav Probably Remi got it right, OP has confounded the concept of dominance with one of high frequency.

You are confounding the concept of dominance with the one of high frequency. The dominant phenotype might be at lower frequency than the recessive phenotype.
Dominance

Dominance in genetics is a relationship between alleles of one gene, in which the effect on phenotype of one allele masks the contribution of a second allele at the same locus

Trait frequency
Let's imagine a case where A is dominance and a recessive. Let, $f$ be the frequency of A alleles in the population. The frequency of individuals that have the dominant phenotype is the frequency of AA individuals plus the frequency of Aa individuals. Under Hard-Weinberg assumptions, the frequency of individuals having the dominant phenotype is therefore
$$f^2 + 2 f (1-f)$$
The frequency of individuals having the recessive phenotype is $(1-f)^2$.
If
$$f^2 + 2 f (1-f) < (1-f)^2$$
reorganizing the in-equation yield to
$$f < 1 - \frac{1}{\sqrt{2}}$$
So under the condition that $f < 1 - \frac{1}{\sqrt{2}}$, the dominant phenotype is present at lower frequency than the recessive phenotype.
If the calculations were unclear to you, then you should have a look at the wikipedia article of Hardy-Weinberg principle.

@AnamikaGhosh As you have not reacted yet, I suppose I may fail to answer your question. If there is anything unclear, feel free to comment on it.


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Is there a resource for comparing categories of life along quantifiable dimensions such as species diversity, geographic range, total mass, etc?
Ideally what I would like is some sort of interactive, sliceable tabular data along the lines of my examples below. The curious individual specifies the level of taxonomic rank, e.g. Kingdom or Class etc., and then can choose to populate several rows from within that category with data on that category's "successfulness" as measured in various ways (of course all the data fields would be estimates)
CLASS        # OF SPECIES  TOT MASS   TOT RANGE    # INDIV.  # CELLS PER INDIV.
Insecta      ???           ???        ???          ???       ???
Mammalia     ???           ???        ???          ???       ???
<click to add a row>

But the user could select a different granularity, so e.g.
FAMILY       # OF SPECIES  TOT MASS   TOT RANGE    # INDIV.  # CELLS PER INDIV.
Formicidae   ???           ???        ???          ???       ???
Felidae      ???           ???        ???          ???       ???

The goal would be to be able to put "superlative" claims about various categories of life into context. I often read claims of a ____'s (species', genus', etc.) success based on one of these or other estimates, but have no intuitive way of attributing an absolute context to the number reported.
Furthermore, such a table / database would just help me form a clearer picture in my own head of "all the life out there" (that we know about). For example, if I wanted to learn all there is to know about every species of "cat" (I am on the internet, after all), how many species are we talking about? Probably on the order of dozens, versus thousands or tens of thousands for ants.
So far I've found "top 10"-style lists and the like, but no single unified searchable tabular database.

Just putting this out there: as far as I know, there isn't an available comprehensive database like this... but maybe you (or others on this site?) could kick off putting one together!

If you put "No" as an answer, I'll happily upvote it until someone else says "yes" :P

you've got a deal!


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Do all living humans literally descend from one ape?
In the opening chapter of Sapiens, Harari writes:

Just 6 million years ago, a single female ape had two daughters. One became the ancestor of all chimpanzees, the other is our own grandmother.

Is there evidence that this is literally true? There seem to be two ways in which it could fail:
(a) Weak version---there is an individual last universal common ancestor, but it's not an ape: that is, all humans (and chimps) share a single individual creature as an ancestor, but that creature was not an ape. It was some earlier ancestor whose descendants would go on to be apes.
(b) Strong version---there is no individual last universal common ancestor: if tracing the entire history of life on Earth and assuming some "stopping point" where we saw life emerge as (e.g.) from a volcanic vent primordial soup, we would find distinct creatures emerging simultaneously in a population, with similar but distinct genetic code, from one of whom some species (such as humans) evolved, and from another of whom others evolved.
Is there evidence that neither is the case? First, (1) that there is an individual creature, rather than a population of creatures, from whom all life descended. If that is true, then it follows that all humans have an individual as a common ancestor, since you can at worst follow the line of descent back to the primordial individual. And, next, (2) that the last common ancestor of all humans (and chimps) was also an ape, rather than say some other animal.

Did you read about Mitochondrial Eve and Y chromosomal Adam: https://en.wikipedia.org/wiki/Mitochondrial_Eve

As the answers describe, this quote is true, but the wording is a bit misleading. A better quote would state "One became an ancestor of all chimpanzees," because there were other apes in that population that are also ancestors to chimps and/or humans. But, the quote is accurate in that there was one female ape with two daughters, one of whom is the mitochondrial ancestor of all humans, the other is the mitochondrial ancestor of all chimps. The mother in the quote is the human/chimp mitochondrial most recent common ancestor. These apes likely greatly predate the human/ape speciation event.

Just 6 million years ago, a single female ape had two daughters. One became the ancestor of all chimpanzees, the other is our own grandmother.

Short answer
Whether or not the claim is true actually depends upon the specific DNA sequence you are considering. The claim is true for sequences without recombination (such as mtDNA and most of the Y chromosome). The claim does not hold true for most of the genome and it is therefore misleading.
Long answer
Basic knowledge required
First, if you don't know the concepts of

allele
haplotype
ploidy
selection
genetic drift
segregation
recombination and crossover

, then you might want to have a look at a short introduction of evolutionary biology such as Evo101 for example. The below answer will make more sense to you with some a priori knowledge.
Coalescence
Imagine there is today a population of $N$ individuals. We are going to look at this population backward in time (which is a little bit unintuitive). For simplicity, we will assume asexual reproduction, no recombination, absence of selection (only drift) and constant population size of $N$ individuals. The assumption of no recombination is key here. The other assumptions are details just to make my job at explaining coalescent theory easier.
We start at time t=0 and are going backward in time. If two individuals are siblings at $t=0$, then, it means that in the previous generation, they share the same parent. Therefore, if we connect individual from generation $t=0$ to their respective parents at generation $t=-1$, we see that some group of individuals (the siblings) "coalesce" to fewer individuals (their parents). Individuals at generation $t=-1$ that are not connected to individuals at generation $t=0$ are those who did not reproduce (or who did not leave offspring that have survived until adulthood).
You can keep iterating over generation $-2$, $-3$, $-4$, etc... At each generation, the number of individuals that are connected (that our ancestors) to present day individuals is diminishing as more and more coalescence happen. After a sufficient number of generations, eventually, only one parent will remain. This single individual will be the ancestor of all present individuals.
If you enjoy math, then note that such process is actually a simple a branching process for which it is relatively easy to calculate the expected time (and the whole PDF) to the next coalescent event and the expected time (and the whole PDF) until all individuals in the population coalesce.
So, assuming no recombination, if you consider individuals in a modern population, then you can be sure that all individuals share a common ancestor who is a single individual, at some point in the past.
Incomplete lineage sorting
The process of all individuals coalescing into a single ancestor takes a little bit of time. For recently diverged species (say species A and species B), it is possible that this common ancestor is older than the time of divergence between species. If this is the case, it is then incorrect to think of a mother who gave birth to two individuals, one becoming the ancestor of all individuals of species A and one becoming the ancestor of all individuals of species B. In such a case, we talk about incomplete lineage sorting.
Note that when we talk about 'incomplete lineage sorting', we are generally talking about specific genes as not all genes coalesce the same way when there is recombination and segregation (see below)
Recombination
Now the trick is that in the presence of recombination, different sequences coalesce differentially. It also means that when you look at two sister species, some sequences can show incomplete lineage sorting while others don't.
The presence of recombination therefore makes the claim false!
Do we recombine?
Yes, all of our genome recombines to the exception of two sequences

mitochondrial DNA (mtDNA)
Y chromosome not including the Pseudo-Autosomal Region (PAR)

mtDNA is maternally inherited (without crossover) and transmitted to all offsprings, while the Y chromosome is paternally inherited (without crossover) and transmitted to sons only.
So, is the claim true?
mtDNA
It is true that there was an ape who had two daughters. One daughter's mtDNA became the ancestor of all mtDNA we have in humans today, the other daughter's mtDNA became the ancestor of all mtDNA that exist in chimps populations today.
Of course, this daughter is the common ancestor of all modern mtDNA but is not necessarily the Most Recent Common Ancestor (MRCA). In humans, the MRCA to all modern mtDNA is called Mitochondrial Eve (mt-Eve or mt-MRCA).
Y Chromosome
The same claim is true for the Y chromosome (although I am not sure there was really not a single recombination event happening on the Y chromosome since). The MRCA to today's all Y chromosome is sometimes called Y-chromosomal Adam (Y-MRCA).
The names 'mt-Eve' and 'Y-chromosomal Adam' have of course been chosen in reference to the creation myth of Abrahamic religions.
Rest of the genome
The Y chromosome and mtDNA together represent less than 0.2% of our genome. The rest of our genome does recombine.
The claim does not necessarily hold true for 99.8% of the genome. I would therefore tend to think that the claim is misleading at best, wrong at worst.
Adam and Eve
We can call Adam the MRCA of all Y chromosomes today. Only Y chromosomes, not the rest of the genome. We can call Eve the MRCA of all mtDNA today. Only mtDNA, not the rest of the genome.
Of course, Adam and Eve did not live in the same time period and did not live at the same place. Adam and Eve never met. And of course, there were plenty of other humans around. They are in no way the first two humans.
Other popular source of knowledge
PBS Eons - The Two People We're All Related To

This is interesting. I will read more. I am struggling intuitively to understand the distinction between descent of particular DNA components versus of whole individuals. Shouldn't the question be answerable just by looking at a "tree" of individuals, without having to consider DNA? We might need godlike powers of historical observation, but if we had them there would be an answer at the individual level. So the DNA story may substitute for the lack of godlike history knowledge, but should it not ultimately tie back to individuals? (1/2)

(2/2) I.e., not who is the ancestor of which Y chromosomes, but just which individual(s) is/are the ancestor of which individuals. Separately, I'm confused about the coalescence argument. Consider times t = 0 ... N, and two individuals A_0 and B_0 at the "dawn of life," and each individual X_t asexually produces a child who will live at X_{t+1} and then dies. Then today I could have two individuals A_N and B_N who do not share a common individual ancestor. I believe you that this counterexample fails, but I don't clearly see what evidence we know that establishes its failure.

@Philip remember sex is involved with most individuals, you have two parents, 4 grandparents, 8 great grandparents, ect. As you go back eventually every individual in the population that reproduced is your ancestor. the ones that did not reproduce didn't pass on their genes. For a lot of asexual organisms "individual" as a concept kinda breaks down, a bacteria splits in half forming two, which daughter cell is or is not the same individual as the parent?

there might be a woman who first had the mutation that created the gene common to all mitochondria in humans, but she had to have sex with someone, and so do her children and both of them has to have parents, and grand parents, and so on and so forth. As you go back it becomes increasingly more likely with each generation that they will have an ancestor in common, If you go back far enough they basically have to have common ancestors because the population size is finite but the but the number of ancestors increases exponentially. most importantly.

It is easy to describe a scenario in which there is no single individual who can be called "the" ancestor of all individuals in a much later generation. Let's say there was, indeed, one individual female who had a mutant form of mDNA that occurs in all of us now; and also let's say that that particular mutation never occurred again (a BIG assumption!).  Indeed that female would be an ancestor to all of us; but certainly not the only ancestor. That one female's daughters and sons each carried only half of her genetic information; the other half came from their father(s); and each of those fathers had their own mothers.  Each of us is a genetic mosaic of a very large number of individuals.
Even if all humanity descended from one tribe of early hominids, with no cross-breeding between tribe members and outside tribes (very unlikely), we would all very probably carry genes contributed by almost all of the members of that tribe.

"Some of the information contained in this post requires additional references. Please edit to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted."  Please be more specific.  Which assertions require references?  This is very basic genetics.

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If a tortoise lost its shell, would it be naked or homeless?
We often call a snail's shell 'house'. But there are also naked snails (=slug).
What about tortoises? Is their shell like a house or an important part of their body? If a tortoise lost its shell, would it be naked or homeless?


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Some facts about the chameleophant please
Can you give me some facts (where it lives, their size etc.) about the chameleophant?
Can't find it on google...

I do not think you posted the question in good faith BTW, a simple google image search for "chameleophant" or a reverse search using the image will lead you to the website.

I'm voting to close this question as off-topic because this is not the place to post jokes, although I hesitantly admit I almost liked this post. Almost.

@AliceD I like your name

Kind of fits your image doesn't it ;-)

It does not exist. It is a photoshopped image. This is the original image which was used to create it:

It is listed on some websites with other photoshopped images, such as this one:
https://www.planetacurioso.com/2013/05/27/como-serian-los-animales-combinados-con-otros/

Okay thank you but why doesn't it exist?

@Squareoot Because evolution favors practical bodies. Look at the poor bugger, how would it shoot out its tongue at an insect if there was a trunk in the way? Duh...

+1 because you somehow managed to find the original pic. Clever. However, in the future, please flag this sort of questions and refrain from answering, as it encourages other users to post similar crap.

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What is this insect found commonly in coastal India?
I have lived in two cities on the western coast of India and I have seen quite a few of these insects(?) in both places.

It basically has an outer cocoon of sorts, which looks a lot like dirty lint. The actual insect is a small wormlike creature at the top of the cocoon. It almost always tries to keep climbing up walls and when it dies, it remains stuck to the wall from its topmost point. The overall length of it, including the linty cocoon is about half a centimeter.
Can someone tell me what these are and if I need to actively avoid them or prevent their appearance in my closet?

Related: Identifying a creature that appears to be a worm wrapped in a cocoon, What is this black and white worm in a white case?,  Help in identifying an unknown arthropod, What insect is this? (India), Identify this smooth-cocoon worm from Southern India, Small worm living in some kind of cocoon......

Related:  What is this animal that hides in dustlike structure?, What in the world is this critter?, What is this hard shelled insect in my house?, What is this insect found commonly in coastal India?, Insect identification - pantry moth vs clothes moth


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How do ants follow each other?
I was observing ants in my house.They all were going in a straight line and also some of the ants were coming back through the the same line.
I took some water and rubbed the line with my finger, then the ants were not able to follow each other. Looks like they were confused.
My assumption is that they may had secreted some chemical .
Am I right ?
If yes, then which chemical is that and how it is secreted?

The chemical we are talking about here is called pheromone, trail pheromone to be specific.

A pheromone is a secreted or excreted chemical factor that triggers a social response in members of the same species. Pheromones are chemicals capable of acting outside the body of the secreting individual to impact the behavior of the receiving individuals.1

Pheromones are of mainly 9 types (13 exactly, but 4 not so common) which are:

Aggregation pheromones
Alarm pheromones
Epideictic pheromones
Releaser pheromones
Signal pheromones
Primer pheromones
Territorial pheromones
Trail pheromones
Sex pheromones
Nasonov pheromones
Royal pheromones
Calming pheromones
Necromones2

Ants, and many other animals, use trail pheromones to mark their trail as a guide for others in their gang. Other ants, catching the signal of trail pheromone, follow the way it goes and reach their gang leader. Trail pheromones are volatile compounds, so it is not very likely that you would see ants following the exactly same path tomorrow or a week later. All ants release trail pheromones, so as long as ants are going through that path, the trail signal will keep getting stronger and will also tell lost ants "Hey, bro! We are going this way. Don't you want to join us?" See, for example, here3:

In the beginning, different ants follow different paths, but as soon as an ant finds the shortest path, all ants join it on that path, due to which pheromones on other paths evaporates and finally, they all walk in straight line.
Of course, trail pheromones are very useful for organisms who have lost their way home, but you know, other organisms, like their predators, are not just sitting and watching them. Some predators can also catch pheromones and find out where the whole team is going, to attack them all at once. Such chemicals are known as kairomones. See this4:

A kairomone is a semiochemical, emitted by an organism, which mediates interspecific interactions in a way that benefits an individual of another species which receives it, and harms the emitter.

Semiochemical is just a type of pheromone which a species X releases, but a species Y can also respond to its presence. Its just like when you walk on road and say "Whoa! Seems like a pizza delivery van just passed by" (obviously, smell of pizza is not by a pheromone ;)
The trail pheromones released by army ants can also be detected by a blind snake or a forest beetle, leading it right inside their nest. Obviously, all semiochemicals are not bad. Chemicals like synomones (helping both species) and allomones (just the opposite of kairomones) are also present5, but they are beyond this question's scope.
References:

 Medical Definition of Pheromone
Types of Pheromones - Wikipedia
Life in Wireframe - Ant Algoithms
Kairomones - Wikipedia
These Pheromones Get The Animals That Secrete Them Killed

Just curious, but why could the smell of pizza not be a pheromone? Smells are just chemicals that get into our nose and are interpreted by the brain. And the smell of pizza can change behavior :)

@DrZ214 It's not a smell generated directly by the human body in order to affect the behavior of other humans.  Being who we are, of course, you could make a case for the pizza parlor that arranges to have the kitchen exhaust vent blow into the sidewalk using the smell of food in the same way that ants use attraction pheromones.

@DrZ214 simple, because its pizza, not Pizzacibus caseus ;)


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How to determine the fastest metabolism ?
Which is the fastest metabolism ? Fructose metabolism or Glucose metabolism

Can you please add some more details on what exactly do you mean by metabolism?

I meant Fructolysis and Glycolysis which is the fastest one ?

in vivo or in vitro? there are a lot of variables that affect metabolic flux in vivo - this is NOT a straightforward question.

@petersmith yah, but it was asked in our and semester paper.


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Have evolutionary biologists ever done anything like this?

Pick a protein that you claim evolved.
List the mutations that you claim happened during the evolution of the protein.
Pick one of these mutations.
Prove that it could happen in nature and produce a viable organism.

This seems like a way to test evolution.

Try looking at the long term E coli experiment, they have even show predictable and more importantly experimentally repeatable evolution. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0014184

incorrect they showed evolution quite clearly. I also reccomend the research on evolution in response to changes in the  the thermal environment http://myxo.css.msu.edu/PublicationSearchResults.php?group=ve or the ones on antibiotic resistance http://myxo.css.msu.edu/PublicationSearchResults.php?group=ar

No they showed a change in protein expression quite clearly, if you are looking for a change in the protein structure I suggest the work on nylonase. https://www.ncbi.nlm.nih.gov/pubmed/17512009 including it induced occurrence in a different bacterium, https://www.ncbi.nlm.nih.gov/pubmed/7646041

If you think the sudden emergence of a new protein from nothing is predicted by evolution you don't understand evolution, nylonase is a different protein sequence with different structure and function, produced through a known mutation in the DNA sequence of a different protein. I honestly don't know what you are asking for at this point.

@John this "lad" obviously doesn't know anything about biology, but also doesn't want to learn (at least he doesn't show the humility typical of a real apprentice).

I have accused you of nothing. I am trying to ascertain what you are asking for. Now however that you have deleted your responses that prompted the statements shows you are only interested in an argument and not information. you have been given an example that fits your exact criteria as stated. so either change your criteria to reflect what you are actually asking for or indicate why you think it does not fulfill your criteria or we can only conclude you don't actually want an answer.

How exactly do you believe new proteins evolve? ALL proteins are changes in existing sequences.

I'm voting to close this question as off-topic because it is not a question about biology but a statement of a debating position. As usual with such trolls the final argument is completely vague.

@David AliceD and Chris, I disagree with the off-topic conclusions (and the down votes btw).  I believe this person framed a good question (although showing research would have helped) and deserves a chance for people to answer.  Saying it's "Off-topic" when clearly it's not is not a good response.

@RunzWitScissors — I think the way you can distinguish an on-topic and an off-topic troll question is to ask whether or not the poster really is asking for an answer to a biological question. In this case the answer is no. What the poster is doing is really saying "I think such and such is the key test of evolution and nobody has done it therefore …" If this were a discussion group he could/would have come straight out and said this. Because this is a Question/Answer group he is resorting to this subterfuge. He is abusing this group and we should not tolerate his behaviour.

@RunzWitScissors I have to agree with David. You should have seen all the comments he wrote and later removed. Some are still here, so you can have an idea of the situation.

nylonase.
nylonase is a different protein sequence with different structure and function from its parent protein. It does something the parent protein could not do. It is produced through a known mutation in the DNA sequence of the parent protein.
ncbi.nlm.nih.gov/pubmed/17512009
this capability shift through mutation has even been induced in other bacterium with similar starting proteins. ncbi.nlm.nih.gov/pubmed/7646041
A review of all three sequence studies can be found here. ncbi.nlm.nih.gov/pubmed/11092619

What do you mean by new mutation? It binds and digests a molecules that did not exist until 1935. To answer your first question yes. https://www.ncbi.nlm.nih.gov/pubmed/11092619

my previous statement does, in addition I have added a reference in my answer.

no they actually can't, the parent protein cannot digest 6-aminohexanoate-oligomer, the substrate in question. Simply increasing the amount of present will do nothing. the Ell' sequence is different than the parent sequence. .

you believe an inactive protein sequence existed to digest a molecule that was invented in 1935? And if you want more information you could look at the papers' references, which identify the separate parent enzymes in detail. Or you could just read more than the abstracts since the parent proteins are identified.

Then you are not reading the papers, at least not past the abstracts, and since you seem unwilling to even bother reading the sources given you I suspect you are not actually interested in an answer. Since comments are not for discussion and you can't articulate a reason the sources given are insufficient, I will leave you here.

"Plus its not even on a gene. Its a plasmid. So its like saying tossing your breakfast around in your stomach is evolution" ________           now have evidence you don't even know what you are asking for. I suggest you take a few biology classes so you know something about genetics and proteins before you ask the question. I also suggest you look up what a plasmid is.

Its an independent set of DNA in the host. So whatever evolution happens on the plasmid is only those changes which the host has already adapted to. In other words not evolution at all.

t makes no sense, a mutation in a gene on a plasmid is the same is a mutation in any other DNA loop. It shows you don't understand bacteria genetics. If you wish to continue this, Isuggest you create a discussion thread.

Yes, actually LOTS of proteins have already been sequenced in many different organisms, and the more related phylogenetically those organisms are, the more similar the corresponding proteins. You may go to the National Center for Biotechnology Information and see for yourself. Or you can work in a lab and sequence some proteins yourself, or just ask to see how people in such labs work.
Even more, we already know some proteins evolve fast, other slowly. Even more, some parts of proteins evolve faster than other parts, and that's related with the function that each part does.
But really, do you think biological evolution still needs to be "tested"? What about Newtonian physics? What about Einsteinian physics? What about the Periodic Table of Elements? Is it because of religion that you accept most physics and chemistry of the last 150 years, but not the main biology from the same period?
So you want an example?
Here is the insulin from Pan troglodytes (common chimpanzee):
malwmrllpl lvllalwgpd pasafvnqhl cgshlvealy lvcgergffy tpktrreaed lqvgqvelgg gpgagslqpl alegslqkrg iveqcctsic slyqlenycn

Here is the insulin from Homo sapiens (humans):
malwmrllpl lallalwgpd paaafvnqhl cgshlvealy lvcgergffy tpktrreaed lqvgqvelgg gpgagslqpl alegslqkrg iveqcctsic slyqlenycn

As you can see, they're very similar, except for a few letters (each letter represents a single aminoacid).
Now let's take a more distant animal, let's say, a pig (Sus scrofa):
malwtrllpl lallalwapa paqafvnqhl cgshlvealy lvcgergffy tpkarreaen pqagavelgg glgglqalal egppqkrgiv eqcctsicsl yqlenycn

Can you see there are more differences now?
The National Center for Biotechnology Information is free for you to research any protein you like, from any organism you like. As I said, there are probably millions, maybe billions, of proteins already sequenced. You can find out which aminoacids became different in the course of evolution, but you cannot come back in time to sequence the animals that lived millions of years ago. But one thing you can do is to search Google for "evidences of evolution" or buy books about basic Evolutionary Biology. I can suggest some if you want.

What's pathetic is your desire to prove evolution wrong, certainly because of religious bias. I may assume you are following the Abrahamic god, because only their followers are so eager to disbelieve biological evolution.

Evolution could be a mythology, like any science, like any religion. The difference is that the evidences are so overwhelming, that you need to close your eyes to them, so you won't lose your faith in a single old book.

Why don't you go to study the subject you pretend to be willing to understand?

Yeah, maybe evolution is wrong. Maybe a god and a goddess together created everything in a way that we believe evolution took place. OK, I can live with that.

Evolution is obviously wrong because it doesn't work even in basic tests like this question.

You should first study biology, learn the difference between apomorphies and plesiomorphies, understand how cladistics works, see how hierarchical are the phylogenetic groupings, among other things, before coming here with all your "certainty". Funny how you religious people never worry about physics and chemistry...


text:
Does self replicating RNA occur in nature?
Do self replicating, independent RNA strands occur in nature? They are often used in laboratory experiments but I have not heard of any wild populations. I mean independent of other organisms and able to reproduce on their own in the environment. I.e., not just viruses or transcription RNA.

I believe what you are looking for is Autotrophic self-replication, and no one has not been discovered, but that makes a lot of sense since the source molecules such a replicator would use are valuable biological molecules quickly gobbled up by bacteria. Prior to the evolution of these bacteria however that would not have been an issue. And as Rodrgo mention the replicator itself would be helpless food for any bacteria. This is why laboratory studies are so important since the can be done in the absence of bacteria.

They probably existed in the beginning of life (on Earth or somewhere else). But any free RNA now would be almost immediately devoured by bacteria or other organisms.
Bacteria are ubiquitous. That's one of the first things you learn in a microbiology course. We do this experiment a few times: open up a Petri dish far from a Bunsen burner, and in a few days you can see how many bacteria and/or fungus colonies have grown in the Agar. Any good microbiology book will show you this. I have none right now with me, but have just found a few links by  searching for "bacteria are ubiquitous" on Google: Understanding Bacteria, The Purple Phototrophic Bacteria, Bacteria in Agrobiology: Plant Probiotics and Public Health and Infectious Diseases.
As for the science studying the origin of life, I recommend The Fifth Miracle: The Search for the Origin and Meaning of Life, by Paul Davies.

While the answer might well be correct, it would be important to have a reference to backup your claim. Also, you should probably address the question of viroids as it is, IMO, unclear from the OP's question whether viroids would be an accepted answer.

@Remi.b References added. IMO, "independent RNA" excludes parasites.

Kind of; they're called viroids. If you mean RNA that also catalyzes it's own replication independent of environment then I'm not aware of any that exist in nature But one could make the argument that all 'life' is simply self-replicating ribosomal RNA which exploits proteins to do other functions and DNA to store it's information more stably.
It's a bit arbitrary to exclude other cells as an environment though.

Including the term "able to reproduce on their own in the environment" rules out viroids and all other parasites.

Their environment is by definition in and around cells, it's an artificial distinction.

"independent RNA" excludes parasites.

I also thought of viroids at first. The question of the OP is a little vague in the sense that it does not really allow us to know whether viroid would fit the category. I would rather disagree that "independent" means "not parasitic" and I would disagree to not consider another cell as not being ones "own environment". +1


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Rosetta - What score does RosettaDock use for I_sc?
I want to get a score using Rosetta for how well a protein binds to a ligand. I understand RosettaDock has a score called I_sc which will give me a number to indicate that.
I found documentation in https://www.rosettacommons.org/demos/latest/tutorials/scoring/scoring about how Rosetta scores structures, but not sure what scoring function RosettaDock uses and whether it is the talaris2014 score.
So the question is what scoring function is used in RosettaDock for calculating I_sc.
Cheers


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What concentration of hydrogen peroxide kills mold?
There are numerous articles online which claim that household 3% hydrogen peroxide can kill mold growing on household surfaces, yet I haven't managed to find scientific studies that show that. My question is what concentration of hydrogen peroxide is sufficient  for killing household mold (defined usually as a reduction of 99% or some other number)?
I have tried searching online for studies regarding the efficacy of hydrogen peroxide in killing mold, and for the minimum concentration of hydrogen peroxide for killing mold, but I didn't manage to really find information on that, though I am not that skilled in finding such information and also don't have much access to scientific literature.

The CDC Guideline for Disinfection and Sterilization in Healthcare Facilities provides a good overview of various disinfectants and their effectiveness against different kinds of pathogens, along with citations if you're interested in more detail.
This document doesn't evaluate the effectiveness of Hydrogen Peroxide against Stachybotrys (black mold) specifically (the CDC specifically recommends Chlorine Bleach for this purpose), but it does describe it's effectiveness as a fungicide. Note that the level of disinfection needed to control pathogenic fungus in a healthcare setting is likely much higher than needed to control black mold in a house, but it can give you a sense of how effective Hydrogen Peroxide is overall:

A 0.5% accelerated hydrogen peroxide demonstrated bactericidal and
virucidal activity in 1 minute and mycobactericidal and fungicidal
activity in 5 minutes [656]
...
A 7% stabilized hydrogen peroxide proved to be sporicidal (6 hours of
exposure), mycobactericidal (20 minutes), fungicidal (5 minutes) at
full strength ... [655]
...
The 7% solution of hydrogen peroxide, tested after 14 days of stress
(in the form of germ-loaded carriers and respiratory therapy
equipment), was ... fungicidal (>5 log10 reduction in 20
minutes),[663]
...
A new, rapid-acting 13.4% hydrogen peroxide formulation (that is not
yet FDA-cleared) has demonstrated sporicidal, mycobactericidal,
fungicidal, and virucidal efficacy. Manufacturer data demonstrate that
this solution sterilizes in 30 minutes and provides high-level
...
Commercially available 3% hydrogen peroxide is a stable and effective disinfectant when used on inanimate surfaces
disinfection in 5 minutes [669]

From this, it seems like you'd want to use accelerated Hydrogen Peroxide, or 7% stabilize Hydrogen Peroxide to ensure fungicidal disinfection. 3% Hydrogen Peroxide is effective against bacteria, but the studies cited didn't test it against fungi.


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what is the characterization of mutant bacteria and how is it done?
I have a task to characterize protease producing bacterial mutants but I have failed to understand what it is and how it is done

Hi, and welcome to the biology stack.  This is clearly a homework question.  While those are okay, they have to follow the guidelines for homework questions.  Please [edit] to show what you've tried, and where the confusion specifically lies.  Thank you!


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Is there a way to chemically detect the presence of Fungus in a sample?
I would like to know if there is a way to chemically or somehow detect the presence of Fungus in a sample?

What kind of sample?

What kind of fungus?

Relevant literature: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968782/

You could test for the presence of chitin, which is a fundamental component of fungal cell walls.  There is precedent for this: https://apps.dtic.mil/dtic/tr/fulltext/u2/a036986.pdf
Chitin is not only present in fungi though, it is also fundamental to insect and crustacean exoskeletons, and the occasional plant species (e.g. Aegagropila).

Don't insects have chitin as well, and aren't insect parts generally found at some level in many foodstuffs?


text:
Is this bedbug or book louse?

Hello everyone.
I have been seeing tiny critters like this one in bed and I started to worryif they are bed bugs. Although they seem different in appearance as well as the fact that they don't seem to bite, I wanted to be sure.
Sorry if the pic is a bit hazy, they are only about 1mm long.
I also did have a bit of a humidity issue since the roof was leaky.
Does anyone know how to get rid of them. I tried different insecticides around the bed and on wooden part of the bed but nothing works.
Could they have settled in my new mattress? :(

this is almost certainly a book louse (aka a psocid). Definitively not a bed bug. See Insect identification - Is this a bedbug?

The pictures aren't very clear, but I would put this down as a book louse, not a bed bug nymph, as the body is quite elongated, which is atypical of the bed bugs and more typical of book lice.
Book louse:

Bed bug:

Courtesy of  bedbugger.com.
Check out also this page from the University of Minnesota Extension; the picture nicely matches the photo you posted in body shape.

Not book louse.

Yes the OP's specimen is most likely a book louse. @totaredom, I agree with your post. As a side note: your source is not very reliable, and I would suggest avoiding its strict usage for support for an answer. Many more reputable resources exist that could more adequately corroborate your answer.

@theforestecologist Yeah, thanks for pointing out.  Was in a bit of a hurry, I'll admit.

Great update with a reputable source. Thanks. +1

@Muze then what is it by you? Bed bug?


text:
Trophic levels and energy loss
Just a general question about trophic levels. Traditionally, it's thought as much as one order of magnitude of energy is lost as one moves from trophic level to trophic level. I am confused here since it seems to me the energy content of certain primary consumers is more if not equal to an equal number of producers. Take a 1 acre lot of grass vs a 1 acre lot of cows; surely the calorie content in the cows is more than that in the grass no? A one ounce cut of beef has more calories than an ounce of grass. I could imagine for plankton or insects, maybe the energy content is not as conserved since they can store less energy and eat less. So my question is whether this one order of magnitude drop is a rule or just a 'rule of thumb' or if I'm framing the whole thing wrong.
Thank you

1 acre of grass will not feed 1 acre of cow. in fact 1 acre of grass feedson good grazing on average 1 cow.  An acre of grass produces about 10,000lbs of grass dry matter in a year. which feeds 1000lbs of cow for the same time.

To second @John, standing biomass $\neq$ to production. Grass production is $>>$ consumer production. Because grass is consumed and turned into consumer biomass (in this case, cattle), and because the cattle aren't being consumed, the standing biomass is greater in the cows than the grass.

Also equal cuts of grass and beef have about the same calories, humans just can't access most of the calories in the grass.


text:
If you suspended your DNA like a rope in its 6ft full length, could you feel it if you waved your hand through it?
Maybe a silly question but I was wondering about this.  Trying to understand how small things are.
I have read that the DNA in a single cell if stretched out, would be about 6 feet long.
If you actually stretched it out and had something hold it - so that it was n a vertical line from about 6 ft to the floor, and then

would it cast a visible shadow?
if you waved your hand through it, would you be able to feel it?

Welcome to Biology.SE: I'm voting to close this question as off-topic because this is a question of physics and the strength of chemical bounds but not so much of biology.

@Remi.b I think we might be a bit overzealous in voting to close/migrate questions that could be appropriate here. I'd recommend we keep it open, I don't think it is any more relevant at physics or chemistry.se than it is here.

You should post this at http://physics.stackexchange.com Briefly, you should consider the fact that the width of the strand is an order of magnitude smaller than the wavelength of light, so even at very close range you won't get a shadow. Even much wider obstacles won't cast a shadow some distance away, and even if a small but much larger object than the DNA strand geometrically covers a light source, you may not get a shadow due to diffraction. If the angle subtended by the strand is smaller than the wavelength of light divided by the diameter, you'll see light diffracting around it.

The energy needed to break chemical bonds is of the order of a few eV, so, you won't feel any resistance as your hand moves through a DNA strand.

@BryanKrause Ok, I retracted my close vote.

I don't see why people are retracting close votes. This question has nothing whatever to do with biology. At the least it should be migrated to Chemistry or Physics or somewhere where it would receive the scorn it deserves. Trying to understand how small things are indeed! Yes it is a silly question.

What on earth do you mean by "wave your hand through it"? Through what? the two strands of the double helix? I think you must be on the wrong site. Try SE Science Fiction and Fantasy: http://scifi.stackexchange.com.

Research on tactile detection has found humans can detect wrinkles in a surface on a nanoscale. One could argue that we may be able to feel a strand of DNA.
However, this research found only wrinkles of 10 nm were detectable. Therefore it is unlikely we would detect a DNA strand by simply touching it, considering DNA has a radius of one nanometer radius (10 ångströms).
We still may feel a pull of the strand depending on the tensile strength and bond strength but I'm not sure how those values relate to human perception.

I originally thought it might be likely that the covalent phosphodiester bonds holding together the DNA backbone may not be able to support the weight of the polymer chain. I did a few napkin calculations to investigate the issue. Here is my analysis:
The nucleotide at the bottom of the chain has a certain very small weight, and will probably not break the bond to the nucleotide above it. The two bottom nucleotides weigh twice as much as the single bottom one, but that also probably won't break the bond above them. If you keep going up with this logic, you might reach a point where some number of nucleotides has enough weight to break the covalent bond above them, and that chain of nucleotides would fall to the floor (making a very tiny puddle).
The bonds in the sugar-phosphate backbone are: $...O-P-O-C-C-C-O-P-O...$ (just a random bit of the chain, where the carbons are 5', 4', 3' of a deoxyribose sugar). The lowest bond energy, thus the most easily broken, is $P-O$ at 335 kJ/mol (Ref). I'm taking this as this how much energy is required to break the DNA sugar-phosphate backbone (in a single place).
An experimentally derived estimate of the linear density of double stranded DNA is $2.1\cdot10^{12} \frac{g/mol}{m}$. So every meter of DNA weighs about a trillion g/mol. Does this sound like a lot? It's because that is the meter-weight of one mole of DNA helices. The linear density of one molecule of DNA helix can be found by dividing by avagadro's number: one molecule of DNA has a mass of $3.5\cdot10^{-12} g$ per meter.
Let's take our vertical strip of DNA and imagine it is divided into two segments: an upper segment held by some vise, and a lower segment which dangles freely. The two segments are connected by a covalent bond of the sugar-phosphate backbone, specifically a $P-O$ bond. The lower segment has some mass $m$, and its weight $mg$ exerts a force against the bond ($F=mg$).
The bond requires energy $E=335 kJ/mol$ to break. This energy can be provided by the lower segment doing work to break the bond. Technically this work would be done by the force of gravity on the lower segment, which releases energy if the segment is moved closer the center of the earth. But the segment will only fall toward the earth of the energy released by that process overcomes the energy barrier $E$ of the bond holding the segments together.
Work is force times distance (roughly speaking), so what distance will the lower segment move in the process of breaking the bond? I think 1 angstrom (about a bond length) may be a reasonable approximation. That is, if we stretch the $P-O$ bond (which is already around 1.5 angstroms long) by 1 angstrom, it should be reasonable to say it is broken and the atoms will not re-attract each other (see Bond Dissociation graphs for details).
So! Our energy $E = 335 kJ/mol$ to break the bond will be supplied by work $W=Fd$, performed by the force of gravity $F=mg$, which acts for a relevant distance of $d=1$ angstroms $= 10^{-10} m$:
$$E=W=Fd=(mg)d$$
The mass of the lower segment is $m=\rho l$, where $\rho=2.1\cdot10^{12} g/mol/m$ is the linear density of the DNA segment and $l$ is the length of the segment. The question we should ask is "how long must the lower segment be for it to have enough weight to break the bond?" Well...
$$E=mgd=(\rho l)gd$$
$$l=\frac{E}{\rho gd} \\
= \frac{335\cdot10^3 J\cdot mol^{-1}}{(2.1\cdot10^{12} g\cdot mol^{-1} m^{-1})(9.8 m\cdot s^{-2})(10^{-10} m)} \cdot \frac{kg \cdot m^2 s^{-2}}{1 J} \cdot \frac{10^3 g}{1 kg} \\
= 1.6 \cdot 10^5 m$$
So, according to my admittedly crude approach, a segment of DNA would have to be on the order of 100,000 meters long to weigh enough to break the covalent bond holding it to the rest of the chain above it. I suppose this is a testament to the powerful strength of covalent bonds (or I've made some grave error somewhere in my physics). So my calculations suggest a 6-ft segment of DNA (magically extracted and assembled from trillions of humans cell) should have no problems holding together when you grip it in a tiny vise and hold it vertically.
I realize this was not exactly your question, but it was a practical consideration that I found myself investigating, and I figured I'd share my results.

I have a sincere question. Did you consider the resonance effect of the phosphodiester linkage when you told the P--O bond energy was 335kJ? There would definitely be some resonance by the negatively charged oxygen. I'm sure that this would increase the bond dissociation energy, but not sure by how much though.

I did not consider it, but I'm not certain it is relevant. Here is a diagram for reference: (http://s3.amazonaws.com/chegg.media.images/board/681/68166991-56d8-47ef-8ccb-7a36b44d9e97-original.png) On a given phosphate, the two oxygen atoms involved in the sugar-phosphate backbone are neutral, and participating in resonance would require them to become positive. The negative oxygen is much more likely (indeed, guaranteed) to participate in the resonance with the doubly-bonded oxygen, but neither of those last two oxygen sensor are involved in the bonding arrangement of the backbone.

Nice! I think the calculations are reasonable.  I did something similar for a polyphosphate chain and found that its P-O bond should support an even longer polymer, about 1000km. And DNA should have higher linear density than polyphosphates, so your numbers make sense. I guess this is the reason for all the hoopla about nanomaterials --- pure molecules have incredible tensile strengths. (Yes, it's not really biology but it is kinda fun :)


text:
Do eye's muscle share the same nerve?
When I try to rotate my eye, both of my eyes will rotate the same amount and in the same direction (obviously).
I'm wondering if it is possible to control each eye separately. I've never seen anyone that can do this (except some pics on the internet which I'm not sure if they are digital edits simply for fun).
Is it possible? If not, why? Is it because they are both controlled by the same nerve? Or is it simply because we are not used to it and it's super difficult (but possible)?

Each eye is controlled separately. Three cranial nerves emerge at the brain for each eye to control the so called extraocular muscles. That we usually move both eyes in one direction is due to that our brain is trained that way. Nonetheless, we sometimes move each eye individually, for example when looking at an object that is very close to our face (convergence). I wonder that you have not noticed it on yourself, since it is a pretty common eye movement. Further, you can train your brain to perform other, rather unusual movements, as you can see in this video.

Ops thanks for the tip! I forgot about convergence, since I was busy thinking about moving them both outside.

So it's like when you play Mario and you instinctively start pressing B when you press over. You don't think about it, you just do it!

There are basically four different types of eye movements:

smooth pursuit (think about following a moving target with both your eyes, note how smooth the movement is)
saccades (think about moving your eyes without fixation on a specific target, note how jerky the movement is)
vergence (the other answer mentioned "convergence", this is an example of a vergence movement)
vestibulo-ocular movements (these are mainly reflex movements which depend on the "position-sensing" apparatus of the inner ear)

The motor control of the eyeballs (globes) is mediated in a fairly complex way via the third, fourth and sixth cranial nerves. The coordinated movement of the eyeballs is mediated neurologically in a really complex way involving multiple brain and brainstem centres (nuclei).
To explore this in detail, you really need a good textbook in neuroscience. For what it's worth, I've found a web reference that covers the gist: https://www.ncbi.nlm.nih.gov/books/NBK10991/


text:
How do I compare bacteria growth curves?
I have bacteria growth curves for 5 different temperature conditions and these were created using %red-light transmittance. How do I compare these growth curves? Should I calculate the growth rate and if so how do I do that?

Please do not create different accounts and ask the same question

If you are interested in learning about the site. You could visit the tour-page for basic informations, the help-page for more detailed informations about what could be asked or could not be.

The other question: https://biology.stackexchange.com/questions/58350/how-to-calculate-growth-rate-analyse-growth-curve-of-bacteria

1) A Bacterial growth curve:
When we provide a favorable medium for bacteria to divide regulary and increase in number, we get what's called a "growth curve", measuring the concentration of cells against time as time passes.
2) Phases:
A) The first phase is called the "lag phase", in this phase bacteria are adapting to the new medium, preparing enzymes etc, to start dividing. Therefore little to no growth is observed.
B) The second phase is the "Exponential growth phase", bacterial cells are well adjusted to their medium and ready to reach full potential, "maximum division and growth" happens here.
C) The third phase is the "stationary phase", bacteria are no longer able to grow or feed, they run out of nutrients, and growth is stationary/zero again. It can persist for a long period of time. (Cell growth=cell death, no actual increase in cell number=stationary)
D) The final growth phase is the "death phase", no nourishment is available and toxic metabolites have been accumulating during the stationary phase, death occurs (death here means that an increasing number of bacterial cells are dying, unlike the stationary phase where the number of cells dead equals the number of cells viable), following cell death (which now happens at a faster rate than cell growth), the cell concentration starts to decline. However, it doesn't really reach zero and bacteria might be able to regenerate again when the conditions are healthy again.
3) Recording bacterial growth using transmittance or spectrophotometer:
As bacterial cells increase in number, the turbidity of their medium increases (depends on the concentration of cells), and the incident light (if you shoot a beam of light across the medium) is more deflected away from the receiving detector (to detect the intensity of light), which makes spectrophotometer a reliable and accurate method to measure cell growth (proportional to the intensity of light detected).
4) How to compare growth curves?
Looking at the growth curve will give some idea of the rate of growth in relation to a standard growth curve or some other available growth curves (compare phases and their durations, the exponential phase, etc). However there is a way to calculate growth curve and generation time (doubling time) from a growth curve.
The difference in cell concentration/difference in time = growth rate constant. Or dN/dt = kN or you may use this advanced equation: log10N2 – log10N1 = k(t2 – t1)/2.303
Simply plot any two random points of time on your curve: the first point is t1, the second point is t2, N1 is the number of cells (cell concentration) at t1, N2 is cell concentration at t2.
Or you can simply use dN/dt = (N1 – N2)/(t1 – t2) and compare the resulting k between curves.
I hope this answers your question, please know that I am by no means an expert on the subject and you may search further or get expert advice if you need to.
References:
Textbookofbacteriology.net
Miller-lab.net/MillerLab
biotek.com/
Academic.pgcc.edu
Web.mst.edu

https://biology.stackexchange.com/editing-help

Calculating maximal growth rates
Maximal growth rates are indeed important to compare, when evaluating the differences between different growth curves. The higher the value is, the fastest is the exponential phase. In order to calculate the growth rate of each curve, you have at least to possibilities:
The quickest and easiest way is to select two points from the exponential phase and use the following formula:
$\mu_{max} = \frac{ln(X_2) - ln(X_1)}{t_2 - t_1}$
where $X_i$ is your measure of cell density (e.g. dry weight, optical density, etc.) at time $t_i$, and $\mu_{max}$ is the maximal growth rate.
Another way to estimate $\mu_{max}$ is to use modeling techniques. A classical model for bacterial growth is the Gompertz model:
$y(t) = A \cdot exp \left[ - exp \left(1 + \frac{\mu \cdot e}{A} (\lambda - t) \right) \right]$
Where $y$ is the measure of cell density, $A$ the asymptotic value of cell density and $\lambda$ is the duration of the lag phase. Tools exist that can help you fit your curves with this kind of model, like the grofit package for R (it's free!). This package can provide you with estimations of $A$, $\lambda$ and $\mu_{max}$, along with the corresponding intervals of confidence (see figure below).

Comparing growth curves
When comparing growth curves, key values to compare are: $\mu_{max}$ the maximal growth rate, $A$ the asymptotic value and $\lambda$ the lag phase duration. One should not neglect one of them over the others. Low $\mu_{max}$, low $A$ or high $\lambda$ are each a sign of possible bacterial stress.

Source of the figure: Kahm, M., Hasenbrink, G., Lichtenberg-Fraté, H., Ludwig, J., Kschischo, M. (2010) grofit: Fitting Biological Growth Curves with R, Journal of Statistical Software (33)7


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Is there a practical upper limit to ploidy?
In my AP Biology class, we were discussing polyploidy, specifically, its deleterious nature in mammals and its prevalence in plants.  We also learned that commercial crops, especially fruit, are often selectively bred for high magnitudes of ploidy.
Fascinated, I googled the subject and ended up reviewing the Wikipedia article to get a little more background info, where I read this:

Polytene chromosomes of plants and fruit flies can be 1024-ploid.[44][45] Ploidy of systems such as the salivary gland, elaiosome, endosperm, and trophoblast can exceed this, up to 1048576-ploid in the silk glands of the commercial silkworm Bombyx mori.[20]

From this, I have three questions. The first is, is there an upper limit to ploidy that can occur in nature? I understand that polyploids can "lose" ploidy by haploidisation, but is this as common as increases in ploidy? I believe that the answer to this would imply the answer to my first question, however, I could not find much literature in the way of this area.
My second question is, is there an upper limit to synthetically induced polyploidy? Is the Bombyx mori's ploidy arbitrary, or is it at the max that technology can produce? Can it's ploidy be expanded further?
Lastly, does arbitrarily high ploidy serve any purpose in agriculture or science? Is there a threshold where utility is no longer maximized?
Thank you in advance.

Note that it is customary to restrict posts to a single question, which is easier to answer for these complex topics. I'll do what I can here. I'm going to deal with everything at once and then reference pieces in direct reference to your 3 questions.
MECHANISMS OF CONSTRAINTS ON PLOIDY
I think that it's worth separating out some of the different mechanistic ways in which a practical limit can be set for how many chromosome copies you could have.
Another point is that the examples you give in flies and silkworms are organs with high ploidy, rather than whole organisms. It's a lot easier for an organism to have a few weird snippets of tissue with weird ploidy than to maintain that ploidy in the germ line.
Ciliates are weird and instructive:
As another totally insane example of how some organisms have evolved to reconcile this somatic desirability of lots of DNA with a stable germ line, you should look into the nuclear organization of the ciliates, which have a germ-line micronucleus (which is just passed on to future generations) and a somatic macronucleus (which is generated by amplification of the micronucleus and does all the cellular work of DNA). The macronucleus is of extremely high "ploidy" (it's more complicated than that but that's close enough), but the germ line is of a more sensible ploidy.
Some constraints I could think of:
Physical limits:
DNAs are basically huge polymers. Packing polymers into a cell imposes a physical constraint, in the sense that you need to 1) fit all that polymer into the cell/nucleus, and 2) need to still be able to use the DNA for all of the necessary cellular processes. These constraints will vary vastly from organism to organism, based on cell volume, plasticity, morphology, etc.
Metabolic limits:
DNA is expensive to make, energetically and physiologically. It ties up a lot of sugar and nitrogen that you could use to do other more interesting things, like the rest of cellular metabolism. Silkworm silk glands are obviously eye-popping, but I assume that there is some theoretical limit above that million-ploid amount (for silkworms) that would be too much DNA to support. For a little more information see this Mike Lynch paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4697398/
Chromosome segregation limits:
Moving homologous chromosomes to daughter cells is not a perfect process; cells mess it up frequently, leading to aneuploidies and cancers. Some ploidies such as triploid, and presumably higher numbers with 3 as a smallest common denominator, are particularly unstable in meiosis. However, any high ploidy leads to errors at a higher rate than lower ploidies. Look at the ciliate example also. This is I believe the main reason for the "collapse of high ploidies into lower ploidies that you mention.
UPPER LIMIT TO PLOIDY IN NATURE
See all above answers.
UPPER LIMIT TO SYNTHETIC PLOIDY
See all above answers. Synthetic increases should behave the same as natural ones, as we are honestly much worse at getting making things happen than nature itself. Nature will have gotten higher already than we ever will, in all probability.
PURPOSE OF HIGH PLOIDY
See the cost/benefit of ploidy article from above.


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Why is the V/Q Ratio 0.8 not 1?
According to: https://en.wikipedia.org/wiki/Ventilation/perfusion_ratio the ideal V/Q Ratio would be 1.0 because 1 L of blood can hold about 200 mL of oxygen and 1L of humidified air has about 200 mL of oxygen.
However, the actual ventilation/perfusion ratio for the entire lung is described as 0.8. I understand there are regional variations due to gravity, but on the whole, shouldn't the average V/Q ratio be 1?
One thought I had was that because it takes time for O2 to diffuse across the membranes and bind to Hemoglobin, that could explain this loss in efficiency.


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Does the brain have a clock and can it be sped up?
Before i start, I'm an engineer and have very limited knowledge on biology and neuroscience. My question is, does the brain have a clock like a computer where it has a set processing speed?
Clocks in CPUs can be overclocked to increase processing speed and I am wondering if the brain has something similar. The average human reaction time is around 0.25ms, Is it possible to react faster to stimuli and not only react but perceive surroundings faster than others. What I mean is while everyone perceives 1 second to be 1 second long, Is it possible to focus and stretch 1 second out mentally to 3-5 seconds and move/think/react faster as a result?
How could this theoretically be achieved too? BCI headset, Chip implant in the brain, serum or chemically?

It's not true that everyone perceives one second as one second.  It's subjective, of course, and I have no idea how you might actually measure it, but if you've ever been in a seriously dangerous situation, you might have experienced time slowing down.

You have to keep in mind that every generation finds analogies between biology and the 'hot' mechanical technology of the time. Back in the 19th century people would make analogies between living organisms and steam engines. At a high level, this can be useful: steam engines and living organisms both employ feedback systems. Once you get down in the details though the analogies break down: living organisms don't boil water to make steam. In the same way, living organisms certainly have periodic cycles in their biological pathways, but nothing like a cpu clock that synchronizes all activities.

Try to read something about suprachasmatic nucleus and circadien rhythm. Might help.

While the brain is often compared to a computer (sometimes even rightfully), one key aspect people often overlook is that the brain is inherently analog, whereas computers are inherently digital:
All a computer really does in any single operation is to combine 0's and 1's really really fast - and the faster it's able to do that, the faster it will generally be.
A brain however, fundamentally works by combining a multitude of signal inputs with varying strength's and each single operation (encoded by a single neuron) will give output depending on the weighted sum of all inputs.
Such a 'single operation' in itself is reasonably fast, whats make a brain 'slow' is the propagation of the signal to next neuron/operation: Brains are orders of magnitudes bigger than computer chips and instead of metal/wires they use concentration gradients to propagate the electrical signals. Of course it's possible to increase the speed on individual connections between neurons by insulating them, which nature already does.
However, you can't just 'overclock' the whole brain, because there's simply not enough space to add 'full insulation' to every single connection between two neurons (of which there a lot: ~100 billion neurons, with a couple thousand connections each) and because electrical signal propagation by concentration gradients will always be slower than by wires.
I guess if would replace all neuronal connections with metal wires and some concentration gradient to power/voltage/frequency converter using nanobots, you could potentially speed up the brain - or just built cyborgs instead.
Also, not really what you asked  -  but there IS a clock in the (mammalian) brain and changing it speed, will seriously mess with your day/night or sleep rhythm.

The answer to your question could be yes or no, determining how you define "clock speed".
First, the title of the question is partially misleading since when you talk about a biological "clock", most people will assume you're referring to sleep/wake, night/day, or melatonin-related (daily cycle) activity. (Turns out your question is about speeding up neural processing power).
Brains (neural networks) are a highly parallel asynchronous architecture (as far as the research suggests). There's no centralized "clock" - every input-to-output chain reaction happens at the speed the hardware supports. It's well known that this architecture imposes some fundamental limits on humans, the easiest example being reaction time (you can confirm this with a few quick searches). In this regard, the answer to your question would be "no".
Think of a neuron as being a machine with n inputs and 1 branchable output (see https://www.reddit.com/r/askscience/comments/2yl5jh/how_does_one_neuron_with_multiple_synapses_decide/ on how axons implement a single output which can be branched). The neuron's architecture is event-driven on the inputs. This produces 2 main limits: the calculation step (how quickly the neuron handles the event and sends an output signal on its axon), and propagation speed (how quickly the signal travels).
This leaves 2 clear options: optimize the neuron cell for a faster calculation step, or optimize the propagation speed (think of this as upgrading all your 10/100 Mbps cables to 1/10 Gbps).


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Identify this avian courtship ritual
The female drops a twig from high up on a tree and the males have to catch it midair. The female is checking if the males can catch things midair because this species nests on cliffs, and the chicks may fall to their deaths while learning to fly. Apparently, skilled males can catch the chicks midair.
Which species is it?

Where did you hear about it?  Do you know anything else about the bird?  It sounds a lot like an eagel, but it's hard to validate that it's the only bird that exhibits those patterns.

So eagles actually do that? Do you have a source? My friend says this happened in a documentary we watched together, but I have no recollection of ever seeing such a thing.


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Neurons and nerves
What is a nerve compared to a neuron? Is it a collection of axons alone or does it include cell body too? I'm pretty confused of what actually the "nerve" is composed of. I had imagined that the nerve is actually having a no of neurons synapsing together but I guess it's not so.. Pls do make a clear demarcation between a neuron, nerve,  nerve fibre, ganglia, nuclei

@novo  I vote to close the question too

This is a rather broad question, but the categorization is as follows:

A neuron is a cell of the nervous system, its role is the transmission of electric signals.
A nerve is a bundle of axons, meaning that it contains neurons but only part of them.
A nerve fiber is another (and in my experience rarely used) term for an axon.
A ganglion is an aggregation of neuron cell bodies in the peripheral (i.e. autonomous and sensory) nervous systems.
A nucleus is an aggregation of neuron cell bodies in the central nervous system.

As you can deduce from the info above, a nerve is distinct from a neuron and does not include its cell body.


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Can insects metabolize poisons?
I am new to this community, and I was wondering if insects could metabolize poisons. I'm not sure if I use the correct concepts, I simply wonder if insects can get rid of non-lethal doses of insecticides, and live as they have never been exposed at them. I know that human liver does this task for us, but I don't know if insects have this mechanism.

Insects absolutely can metabolize poisons. This is because plants are absolutely chock-full of them, precisely to avoid insect predation, and in return many insects have developed immunities to many of these poisons. Or as this paper "DETOXIFICATION OF PLANT TOXINS BY INSECTS", which looks like it would be the answer to your question if it were free to read says:

It is estimated that all plants
  contain some type of defensive compound (Rhodes
  and Gates, 1976). However, plant defensive compounds
  are not universally toxic to insects (Janzen,
  1979). Since almost all plant species are attacked by
  some insects (Schoonhaven, 1972), it is obvious that
  phytophagous insects have been able to develop
  countermeasures which allow them to feed successfully
  (Jones, 1972).

There are three main ways for an organism to neutralize a toxin: sequestering it where it will not harm the rest of the organism (and conveniently, may make the organism itself toxic to its own predators), excreting it (i.e. getting it out of the body altogether) and metabolizing it, i.e. chemically converting it into safer compounds. Often you will actually get combinations of those.
The first page of the paper sadly does not get into details about the extent to which insects use the third strategy, but it clearly states that they do.
This picture from Wikipedia shows some of the digestive organs that contribute to metabolizing toxins:

Organs that appear to deal with neutralizing toxins include the midgut (13), the fat body (not pictured), the hemolymph (not really an organ, it's the blood-equivalent liquid that all the organs bathe in), and the Malpighian tubes (20), though the latter (the apparent equivalent to our kidneys) probably serve more to physically get rid of the toxins than to metabolize them. From the Wikipedia page :

In insects which feed on plant material containing noxious allelochemicals, Malpighian tubules also serve to rapidly excrete such compounds from the hemolymph.

And from here:

Some small organic molecules are also
  actively transported into the tubule
  lumen by the transcellular pathway,
  including alkaloids (plant compounds
  which may be toxic to the insect).

This PLoS One paper (so, free to read) studies the enzymes that insects use to metabolize some toxins and notes among other things that:

One of the best studied examples is the CYP gene superfamily of Papilio butterflies (Papilionidae), which have adapted to furanocoumarins, the toxic components of their food plants [15], [16]. These toxins are degraded by inducible CYPs that are expressed in the midgut and also in the fat body [17], [18].

and

For Tyria, senecionine N-oxygenase (SNO), a soluble enzyme located in the hemolymph, has been shown to convert the pro-toxic free base efficiently into its non-toxic N-oxide [22] (Figure 1).

(emphases mine)
Another paper, "Chemical detoxification vs mechanical removal of host plant toxins in Eucalyptus feeding sawfly larvae (Hymenoptera: Pergidae)" describes how some sawfly larvae have special mechanisms for getting rid of and sequestering toxic oils, but also says :

The oil sequestration is, however, incomplete and chemical gut content analyses by gas-chromatography (GC) revealed that 1,8-cineole does enter the midgut and is metabolised to hydroxycineole.

Another paper studying a class of enzymes generally associated with detoxification (but note the paper itself is about how those enzymes have other roles as well):

Insect monooxygenases can be detected in a wide range of tissues.
  Highest monooxygenase activities are usually associated with the midgut, fat bodies and Malpighian tubules [9], but again the expression of individual P450s can vary between these tissues [17].

Insofar as insects have an equivalent to our livers it would seem to be the fat body. Like the liver this organ has many functions, including fat storage, energy metabolism and regulation, but also metabolizing toxins. From "INSECT FAT BODY: ENERGY, METABOLISM, AND REGULATION" (free to read):

Whereas many insect tissues have vertebrate analogs, the fat body is an organ unique to insects (77). The fat body is a relatively large organ distributed throughout the insect body, preferentially underneath the integument and surrounding the gut and reproductive organ (36). Unlike the solid structure of the liver, the insect fat body is a loose tissue.

and

Most of the insect’s intermediary metabolism takes place in this organ, including lipid and carbohydrate metabolism, protein synthesis, and amino acid and nitrogen metabolism.

and

In addition to its role related to storage and utilization of nutrients, the fat body is an endocrine organ (65), produces several antimicrobial peptides (44), and participates in detoxification of nitrogen metabolism (74).

And from the other link:

As in vertebrates, the oxidative metabolism is mediated via the tricarboxylic acid (TCA) cycle and the electron transport enzyme systems. The fat body contains enzymes mediating the gluconeogenesis process as well as enzymatic systems with a detoxification role to manage harmful endogenous metabolites and toxic xenobiotic compounds. Detoxifying enzyme systems include microsomal mixed function oxi-dases, in which the cytochrome P450 is predominant, various hydro-lytic enzymes (esterases, phosphoesterases), and conjugating systems.

Maybe it's just a matter of semantics, but if an insect can metabolize a toxin, is it still a toxin to that insect?  There seem to be a good number of instances where species A can happily eat something that is toxic to species B.  E.g. dogs and chocolate, or acorns & avocados reportedly being toxic to horses.

@jamesqf I think it's mostly semantics as you say, but I will note a context in which an organism could be able to metabolize a toxin but it would still make sense to call that compounds a toxin for that organism: consider that the processes that metabolize or otherwise neutralize the compound may be limited. For example humans can metabolize alcohol, but you can still die of alcohol poisoning if you drink more than your liver can handle, and you'd be dying of basically the same thing as you'd have died of if you couldn't metabolize alcohol at all, so that clearly makes alcohol a toxin.

But if you follow that logic, pretty much everything is a toxin in high enough doses, even things like water that are absolutely necessary to life in lesser amounts.

@jamesqf excess water doesn't kill you by overcoming the defense mechanisms you have against water, without which even a little water would kill you. So no, it's not the same logic at all. (Note that I brought up alcohol as an easy go-to poison, and it's a decent example for the point I was making, but "poison" and "toxin" aren't synonymous, and I don't think alcohol is a toxin given the definition of the word).


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Why would evolution favor blue as a color in bugs?
This question arose when I saw a metallic blue - black bug some while ago. I can't remember the species name now, but a quick google search will show that such bugs do exist. I'm down with green and black - camouflage, right? But what is the case for blue color? What kind of an advantage does it provide so that they have survived to this date?

Similarly, you could ask

Why are bees yellow?
Why are some frogs so colourful?
Why widowbirds have such long tails?
Why do peacocks have such a tail?

There are a number of reasons why such traits could evolve. The main reasons are:

Sexual selection (esp. intra-sexual selection when it comes to colors)
Mimicry (esp. batesian mimicry)
Aposematism

I let you investigate further by yourself through reading the linked wikipedia articles.
For the specific beetle, you have seen, it will be impossible to address the question unless we know the species.

Also consider that insects (and their predators) often see different parts of the spectrum than humans do.


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Is a haploid essentially half of a homologous pair?
Is a haploid essentially half of a homologous pair? I understand that a haploid consists of only one set of each chromosome, so does that mean that if that chromosome was replicated the cell would become diploid and have homologous pairs?

Yes, you seem to have understood it correctly. On top of haploid and diploids, there are also cases of triploids, hexaploids, octoploids and others.
For example, some species of strawberries are decaploid (10 copies) (Hummer 2012). Then, there are the extremes. In Entamoeba populations, there can be variation in ploidy level among individuals ranging from diploid (2 copies) to tetracontaploid (40 copies) (Mukherjee et al. 2008)!


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Left-handedness and Right-handedness - Are they genetic?
I have a biology book that states that whether a person will be left-handed or right-handed is determined by the genetic constitutional makeup.
Is this true? As far as I knew, these traits depend on how a person is trained as a child: every child has a tendency to use the left hand first when he starts to write, but if the parents teach him, then it will change to the right hand.
What is the truth?

Not true about the writing.  If a normally left-handed person is forced to write with their right hand (as many were in my youth) the result will be a clumsy kid.

Handedness has, like many traits, a non zero heritability. You now should read the post Why is a heritability coefficient not an index of how “genetic” something is? to understanding what heritability mean.
In short, yes part of the variance in handedness seen in the human population is due to genetic variance.
You will note that footedness is highly correlated with handedness (wiki > footedness).
Note also that today, in the western world at least, it is generally considered unhealthy for the kid to force him/her to use its other hand (as the catholic church used to do). I am not sure what are the evidence for that but it is a totally different question.
References

McManus et al. 2013
Brandler and Parachini 2013
Harmour et al. 2014


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Why do female humans invest more in parental care than male humans, from an evolutionary standpoint?
As the question title suggests, why do female humans invest more in parental care than male humans, from an evolutionary standpoint?
My guess is that the crux of this that males and females have different reproductive biology, but this by itself would not a very satisfying answer, due it not being very comprehensive.

Have you investigated closely related species? Do you know Bateman's principle and the theory of parental investment?

Do you have a source that they do invest more? I have not seen research showing an non-cultural variation.

I am voting to close as unclear until the OP adresses the questions in comments.

"too broad"??? That's a GREAT QUESTION!! How can you erase it? Leave those inexpensive few kB for us to use our brains!

That's a BIOLOGY site. Most evolutionary questions are broad. How can we think biology, how can we think evolution, if "broad thinking" is not allowed? Biology is so close to philosophy, yet you keep pulling them apart!

@BiologyStudent: in Mammals, in general, the long pregnant state, plus the breastfeed, etc causes females usually displaying much more parental care than the males, because they already invested so much. In other animals, like some fish and birds, where the males build and ornament the nest, the reverse is expected.

@anongoodnurse was that too broad for you?

@AliceD was that too broad for you?

@Remi.b was that too broad for you?

@kmm was that too broad for you?

@David was that too broad for you?

And really? All this should need not even 1kB!


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Blastx: from gi to description
I have done a blastx and use the outfmt 6 option, because I want to work in the tables format. When I do this I get subject ids of the type

sp|Q7XJS0|ASHR1_ARATH, sp|Q39547|CUCM1_CUCME,

et cetera.
However, in this blastx output format I cannot find any option that will give me the descriptions of these blast hits.
Could anyone advice me how I can link these subject ids with descriptions of the sequences, e.g., 'amino acid transporter ANTL1-like'? I'd be much obliged.
j

Does the fasta/gb file from which this BLAST database was built have these descriptions in the header? If not take a look here: https://www.biostars.org/p/110000/

You have to map these ids to a file that contains gene description. Usually the GTF/GFF file for that reference genome would have these descriptions.


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In the presence of oxygen after performing a running race, the body works on
a-oxidizing lactic acid
b-oxidizing NADH
c-reducing pyruvic acid
d-ATP molecule decomposition

Welcome . Questions here are required to show results of prior research as described in the [help], particularly the homework policy section. This demonstrates that you’ve taken the time to try to help yourself, saves us from reiterating obvious answers, and helps you get more specific and relevant answers. Please [edit] your question with links to or references to what you've found in your search. For obvious reasons, social media posts don't count as credible sources.


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How does a neutral allele change relative to a nearby allele under selection?
Suppose I'm looking at a gene being selected against (A) that's decreasing at a rate ($\Delta$P). If there's a nearby allele that is neutral (B) am I correct to assume that B will decrease with A at a rate of $\Delta$P*cM?
So for instance, if A and B are .5 cM from each other and A decreases from .8 to .4, will B decrease from .8 to .6 because there is only a 50% crossover rate between the two?

Depends if your trait is dominant, recessive or additive. You should talk entirely in terms of alleles and not as genes as you have to consider the heterozygote case. Your calculation would be correct for a dominant allele with deleterious effects but not necessarily for a recessive or additive trait.


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Rapid Decomposition Of Fruits & Vegetables During Hurricane
A very strange thing (To my mind) has just happened in my home. On the eve of Hurricane Irma, I purchased some food including cucumbers and grapes. I left them in my kitchen area overnight. When I woke up the next day, the hurricane was overhead. I went into the kitchen and noticed a large puddle of water on the floor that smelled of cucumber. The bag I had left the cucumbers and grapes in was at the center of this puddle.
I opened the bag and saw that the cucumbers and some of the grapes had completely disintegrated. It wasn't as though they had decomposed in any normal way. There was no visible fungi and the cucumbers didn't look especially rotted, just mostly gone. Only a small portion of the cucumbers remained. Many of the grapes were in a similar state.
How is this possible? When I bought this produce, it was fresh, not old. They had been reduced to almost nothing in less than 24 hours. I tried researching possible causes for rapid decomposition but normal decomposition of a cucumber (To this point) takes several months. I wasn't able to find a single article or time-lapse that reflected my observation. I've always been very interested in mycology so I set out to find a fungus that might be responsible but I have as of yet been unsuccessful. Could the pressure of the atmosphere during the hurricane have played a role?
If anyone can explain this, I would love to know what happened. Do I have some rare fungi floating around my house? Should I be worried?

If possible, can you kindly include a picture of the grapes and cucumbers?