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Is it possible to induce erysipelas to treat cancer, under the condition that the patient is to be given antibiotics to control the erysipelas?
Dr.William Coley was one of the first to attempt fever therapy on cancer patients. He did this experiment: artificial erysipelas to treat cancer.
Coley injected Streptococcus pyogenes directly into the tumor.
My question is: if we repeat a similar experiment today, (under the condition that the patient is to be given antibiotics to control the erysipelas to avoid the ethical debacle), is it possible to develop this as a cancer immunotherapy treatment?

Welcome to Biology.SE. Ethics (incl. bioethics) is a subfield of philosophy. You should ask your question on philosophy.SE.

@Remi.b I very much doubt this question would be welcome on philosophy.SE

@har-wradim How about Philosophy.SE > Biology progress and bioethics.

@Remi.b Maybe, but I believe we are in a better position to address this question: see my initial attempt.

See also, wiki > ethics. Ethics or moral philosophy is a branch of philosophy that involves systematizing, defending, and recommending concepts of right and wrong conduct.. If you think users of Biology.SE are good at answering this question, then they should do so on Philosophy.SE. Note that there are already about a 100 posts tagged ethics (see here) on philosophy.SE.

My point is that this is more a procedural question: note the "considered", "standards" and "develop ... as ... treatment". The question is not whether such an undertaking would be ethical, but whether it is at all technically possible in the context of todays ethical standards as accepted in medicine and biology.

@har-wradim this is a good point, I now agree with you. I am unsure whether it is on-topic here but it would not be on-topic on philosophy.SE. Maybe Academia.SE would be a place to consider but I don't know. In the meantime I retract my close vote.

I've suggested reopening as the question is now no longer an ethical one, but is more succinctly speaking "Can a heightened immune system influence cancer treatment"? Still, the question needs further references, and perhaps a better developed explanation of the theory behind why such an idea might work.

I'd suggest that the question was closed because it was a question of ethics, I don't think suggesting the treatment is given with antibiotics to avoid ethical issues solves that, you can still just ask whether and how the treatment would work

Before any experimentation on humans, any treatment undergoes an extensive testing on animal models.
Besides, there must be some degree of confidence in the potential curative effect of a remedy in order to start experiments in the first place. An experiment like the one you describe would not be approved by your institute's animal ethics commission (there is such an unpleasant but important thing) unless you prove with some line of evidence and prior knowledge that the suffering of the animals is likely not going to be in vain.
It is now also customary to provide an official approval from the ethics commission during publication submission. [You would not need such an approval for flies or worms, but for rodents (which would likely be your first test object in the case in question) or primates you would.]


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By just looking at an unlabeled picture, how do you know it is a protein?
I'm learning about proteins and need to understand this concept. What makes this colourful ball of squiggles identifiable? Why is it a protein, and not any other biomolecule (like DNA for example)? What are the colours showing? What are the variations in the shape of the image?
Basically, the question is: What is this image trying to tell me about this protein?

This question is unclear. Are you asking "What is this protein?" or "What about this structure makes it a protein?"

DNA is a double helix. This, obviously, is not.

I'm tempted also to say "experience" - for example, to me this is clearly a TIM barrel fold...

@MattDMo DNA was my added example. I think OP wanted to know something along the lines of: "How do people recognise this instantly as a protein rather than any other biomolecule?"

Shapes
This is a common way of illustrating a protein and is often called a "protein cartoon". There are other common ways of illustrating proteins.
This cartoon shows you where α helices are (spirals) and where β sheets are (arrows) which are important structural elements. The strings connecting those structural elements are flexible "loop" regions.
If you want to query this against other structures and see which protein it is, check out PhyreStorm. You'll need the PDB file, not just an image.
Colour
The colouring is also common. The N-terminus (the first amino acid) is coloured blue, and the colours go through the rainbow to red, the C-terminus (the last amino acid in the polypeptide chain).

Even though this question has been answered (and the answer accepted), I want to add something regarding scientific language and convention.
Language in general is a means of communication which allows people to share ideas they have inside their minds. Scientific language is used for sharing scientific knowledge between people, and apart from verbal and written communication, it also uses drawings of all kinds to better illustrate complex ideas that are usually invisible to the naked eye (whether we are talking about molecules in chemistry, biological microsystems in biology, forces in physics, etc.).
The image in question represents the conventional way of portraying a protein structure, and this widely-accepted convention is characterized by certain colors and shapes, as stated in the above answer. I imagine that anyone seeing this kind of representation for the first time would not know immediately that this is a computer rendition of a protein, because no one knows what a single protein looks like before actually studying about it. But once you are told it is a representation of a protein, you accept it and "tag" it in your mind, so that next time you see it, you already know this is what a protein "should" look like.
And the more you study it, the more natural this language becomes for you.

you're pointing something very important to understand to students of science - most of what we learn in classes is not actually the study of the subject, but rather the conventionally accepted languages and modes of representation used by the scientific community to talk about the subjects and convey information.

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Blast databases
I am helping a colleague setup a local blast server. My background is computer science so I apologize if I use incorrect terminology.
Using the NCBI blastn webpage, one of the databases listed is "NCBI Genomes (chromosome)." I'm unable to find this database listed on the database download page (ftp://ftp.ncbi.nlm.nih.gov/blast/db/).
What is the name of this database as listed on the ftp site?

Have you tried contacting NCBI help?

In addition to NCBI, you can also use genomes from UCSC and Ensembl.

With the blast binaries you get a perl script update_blastdb.pl which you can use to download preformatted databases from the ncbi (it's pretty much a script that fetches the data from the location you found, anyway).
With update_blastdb.pl --showall will list all available blast databases and probably refseq_genomic is what you need, unless your query is human data only.
However, that's based on the assumption that your query data is nucleotide data - you might need to choose different databases and tools for proteins
Unlike Maxim Kuleshov claims, the NC and NT accession prefixes don't differentiate between organisms, but genome assembly status, as stated in the linked documentation and the refseq release notes, section 3.8

human_genomic.*tar.gz is Human RefSeq (NC_######) chromosome records with gap adjusted concatenated NT_ contigs and other_genomic.*tar.gz for non-human organisms (more about RefSeq accession numbers such as NC_ and NT_).
You can find more information in the readme file.

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How can I evaluate the hydrophobicity and/or surface charge of a protein?
How should I evaluate protein surfaces in terms of hydrophobicity and surface charge properties of the surface.
Particularly I am looking to compare hydrophobic patches or surface charge between two proteins, from .pdb or Fasta sequences for example.
The goal is to study protein adsorption mechanism in the context of protein purification.

Have you used pymol?

Yes, but does pymol shows a numeric value for total surface hydrophobicity percentage for example?

Yes. You can calculate solvent accessible surface as a fraction of the total surface. Although I'm not exactly sure what "total surface hydrophobicity percentage" is.

I've made some edits to your question to make it more about the biological concepts rather than "what tool is best".

Since you have the structures the best option, in my opinion, is Pymol.
Hydrophobicity
Open Pymol. Load up your protein of choice. Download color_h.py which is a script from the University of Osaka that colours the residues according to Eisenberg's scale of hydrophobicity. Load this into Pymol by File->Run->PATH/TO/color_h.py. Then in Pymol run the following commands

show surface
color_h

Note that the script can be edited to use whatever scales you like. @mimat points you toward protscale and I would suggest the same. The Eisenberg scale is a rather old consensus scale. More up to date scales might be more appropriate in your case.
To start quantifying this, Pymol has tools for calculating solvent accessibility for example.

Additionally PDBSum and PDBe-PISA can estimate solvent accesible surface area.
Surface charge
Vacuum electrostatics
The quickest and easiest way to generate electrostatics is with the inbuilt vacuum electrostatics tools. In Pymol, select the action button (A)->generate->vacuum electrostatics->protein contact potential.

ABPS
Since the Pymol inbuilt electrostatics make a lot of assumptions, for publication it is best to get a much more accurately quantified surface map. However, ABPS is a bit more involved. Read the wiki if this sounds more like what you need.

I think you are after protscale. It gives you a whole bunch of options to predict how your protein will be 'behave' for HPLC purification and hydrophobicity, buried residues, etc.

Protscale is a great tool for sequence analysis. Since we have the structures I think there are more reliable ways to look for biochemically interesting surface patches that take advantage of the 3D knowledge we have.

I agree with you completely, your answer will definitely give a more reliable and complete picture of hydrophobicity. Then again it also depends on the volume of proteins you need to analyse, since the poster was asking about purification you often want something quick and dirty for a lot of different targets.

I see. Good point!


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What do the the different arrowheads mean in a cell signalling diagram?
What do the different arrowheads mean in the figure below? Are there arrows upstream or downstream signalling?

Hi and welcome to Bio.SE! This is pretty standard notation. The arrowhead is a promotion, and flathead is an inhibition.

Hi James! Thanks for the answer! Do you happen to know any resources in general for these notion? and other types of pathway like dotted lines and etc?

Arrowhead interpretation
As I said in my comment and to add to @AlwaysConfused's answer, the arrowhead is a promotion, and flathead is an inhibition.
Typically, any other notation such as dotted lines would be explained in the figure legend of the illustration.
The below definitions are generally accepted and widely used.
But don't take these definitions for granted; there are no strict usage policies for these diagrams.
Different groups may use different nomenclature and symbols.

These definitions were taken from a legend in cellsignal.com.
Upstream and downstream
The arrowheads are not necessarily linked to up and downstream signalling.
Generally, the direction of the arrow indicates upstream/downstream.
However, at a glance, this has even less standardisation than the arrowheads.
Sometimes, like in the example in the question, upstream is generally at the top, and downstream is at the bottom.
Other times it is from left to right, or right to left.
There are many examples of cyclical events which the only way to tell is by following each arrow "path" for a particular signal.

The "normal" (green here) arrowheads stand for a positive effect of the upstream factor or protein on the process or protein it points to. For instance, it means amino acids activate TORC1. Instead, arrows that end with a line (red here) stand for inhibition. For instance, rapamycin inhibits TORC1.

Oxygen, amino acids , energy level and growth factors are activating TORC1 gene (growth factors also cause TORC2 activation).
Then further TORC1 gene  promotes translation, cell cycle and metabolism, but inhibits autophagy. Whereas TORC2 promotes cellular metabolism and cytoskeleton.
Rapamycin and Stress inhibits TORC1.
Green arrow is used to show stimulatory effect and Red flathead  is used for showing inhibiting effect.
These arrows have nothing to do with upstream and downstream signalling.
Read further about this https://www.khanacademy.org/science/biology/cell-signaling/mechanisms-of-cell-signaling/a/intracellular-signal-transduction

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Need help in codon optimization
I want to chemically synthesize a GFP gene for expressing in rice.I am using the IDT Codon Optimization program and found that not all the codons are 100% optimized. Some of them are the 2nd or 3rd in frequency of usage. Also, the stop codon in the gene optimized is the least used in rice. I don't think all the codons can be the ones that are the most used in rice as there is need of translational pauses to get optimal protein expression. But how do I decide which codons are to be used in what positions to get maximum efficiency. Do I just use the automatic codon optimized gene given by IDT or further optimize it manually?
So should the stop codon used be the one which is the most frequently used in rice for proper mRNA termination?
Please help me as I am new to this and want tips and suggestions for getting optimized codons in this gene.

Generally the codon optimization is the most frequent tRNA found in your species of interest. However, your codon must not result in something that disrupts standard molecular biology practices. For instance, if your codon places a restriction site in a unique cloning vector, then the algorithm will just look for the next best codon which does not cause unwanted addition or elimination of a cloning site. Places like IDT will also weigh the cost of the codon vs. the ease of manufacturing in their algorithm (see here.)
What you describe as translational pausing that is 'needed' by the organism to optimize proper gene expression is a consequence and not a necessity of infrequent codons (to my full understanding). See here. That means you don't want to add this translational pausing in optimized gene expression. It is a simply an evolutionary byproduct.
Edit -
To answer your question more bluntly, I can tell you with some experience to trust the codon optimization algorithms from biotech companies like IDT. I find they work very well. Rice is a common enough organism :)

The optimization done by service providers like IDT should be fine because they weigh in multiple factors like avoiding mRNA secondary structures and specified restriction endonucleases. Even I was considering manual editing but then some research on the internet revealed that codon usage is not the only factor involved :)

This is not an answer to the question.

@WYSIWYG Why not? It seems to be poorly supported, but it does seem to answer the question.


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Fe(II) and Fe(III) transport from rhizosphere across plasma membrane
Does the graminaceous plants have passive uptake of Fe(II) via a passive Fe(II)-transporter enzyme? Or it it only dicots and non-graminaceous plants that have the Fe(II)-transporter enzyme? Also, can Fe(III)-reductase reduce Fe-EDDHA (Ethylenediamine-N,N'-bis(2-hydroxyphenylacetic acid)) and Fe-DPTA (diethylene triamine pentaacetic acid) without the cost of energy?
Best regards,
Mathias


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Server for protein structure prediction for multiple sequences
Does anybody have any idea about any online server that takes in multiple amino acid sequences in fasta format and outputs the 3D structure of the input amino acid sequences in the form of helix, sheet and coil? I searched but could not find any. There are servers that take in 1 sequence. I want to get the structure of multiple sequences together...

Why do you want multiple sequences together? What is the problem with doing one after the other? Is there any additional aspect to this that is not evident in the question?

the number of proteins is huge, so I wanted to know if there is any website that allowed batch processing

I am sure some API would exist. What is the server that you are using? Did you check its manual? You can also write a script that can do one-by-one submissions and retrieval.

Also when you have lots of data you should get program not waste time with server.

@Mithoron with this kind of data and computation, that's easier said than done

@Maljam What kind? It's not like OP asks specifically to get native structure with 100% accuracy

If you are only looking for secondary structure prediction you could try the JPred-server API.
On their website they refer to a script that

provides a JPred user with advanced functionality for an easy submission of hundreds of JPred jobs in a sustainable manner.
  […]
  For full details on the code, how-to, and for download please check Fabian's GitHub repository page.


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Secretion in Gram negative bacteria
Among the 6 secretion systems in bacteria, can these 6 ways be sorted out in the order of how harmful it is to the human host? Like say type 3 is highly virulent so that comes first, but I don't know about the rest of the systems. Being a computer science student, I have failed to understand the Wikipedia article to derive this order. Does a discrete order even exist? Can anyone answer this question?

Theoretically there are two very basic things to consider in judging virulence for the secretion systems:
a) Can it secrete into any human cell? (If not, chances of being virulent are smaller, but not zero as whatever is secreted in the environment of a cell could also be harmful for the cell.)
b) Does it secrete some agent (protein, RNA, molecule), which is potentially harmful for a human cell?
a) alone is not sufficient for it to be virulent if b) is not also given.
(As it could inject something in a cell that the cell can handle without a problem.)
b) alone is not sufficient, as it has to get inside the cell somehow. Although, b) alone can work, if the agent has another way to get inside a cell or to harm the cell from outside.
So, generally, without knowing ALL the bacterial secretion systems and secreted agents, it is impossible to decide if one secretion system (alone) is always, sometimes or never harmful.

So these 6 categories does not include all the secretion types?

All we know, I would say. But that was not what I meant to point out. The mere existence of a secretion system does not mean there is something harmful to be secreted, or that it can be secreted into a human cell. Even if the "generalised system" is said to be able to secrete into a human cell, there might be mutations in some bacteria which change it into being less or more effective. Even if the secretion system is not mutated, the bacteria might need additional systems to adhere to a cell or adhere more strongly.

I think I did not quite get this answer. I think the questio is much easier than you say. In general the majority of the secretion systems are know to be used by symbiotic and pathogenic bacteria to interact with other bacteria and eukaryotes. Now, there is a huge amount of literature on the T3SS. It is used by pathogenic bacteria to alter immune response and cytoskeleton of the host and allow the delivering cells to colonize the host cells without being digested.

So if you refer to pathogens, well then you can consider the T3SS as an archetype of virulence factor. Instead, T4SS, T5SS and T6SS can also have other function besides virulence. So in general is the bacteria you are dealing with is described to be a pathogen, and has a T3SS, 99% this T3SS will be involve in virulence.

The presence alone of the SS does not allow you to define if a bacterium is pathogenic or not, but knowing the lifestyle of the bacterium you can be quite sure that if these systems are present, they are used for virulence. Just keep in mind that T1,2,4,5,6 can have additional function than virulence.

Additional comment, recently was discovered a T7SS, so no the 6 you mention is not all we know. Look the review in my previous answer.

I think you cannot find a better answer then the following review:
http://www.nature.com/nrmicro/journal/v13/n6/full/nrmicro3456.html
It was published in 2015, and it gives a good overview about the secretion systems. Anyway, T6SS can also be virulent. Vibrio cholerae can use an effector of this SS to cross-link actin in the host cell and modify its morphology and its cytoskeleton behaviour.
In general I think that there is not a general order of virulence, also because the T3SS was discovered long ago. Whereas, the T6SS just recently, so the amount of information about its function is still somehow limited.
Hope this helps.


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Must I HPLC-purify my PCR Primers for amplicon sequencing with PacBio SMRT?
I would like to order some primers for amplicon sequencing. I am using universal tag primers (unusually long 30-mers recommended by PacBio for SMRT, both F&R) + barcodes (16-mers).   The resulting order of 192x46bp oligos is prohibitively expensive, because of the recommended HPLC purification. The increased expense is related to purification and to the increase in minimum scale (amount) required for ordering.   My question is this: what are the worst-case scenarios (and likelihood thereof) if I do not HPLC-purify primers for PacBio SMRT sequencing?  I am generally looking to make the process of sequencing heterozygous RT-PCR products less expensive, so additional advice in that vein would be terrific, especially from experienced users.  Additional, minor and clarifying side-questions. The PacBio recommended primer, the Universal Tag 30-mer primer seems a bit long to me, and possibly unnecessarily so. Does anyone know why they would insist on a 30-mer? It's a bit irritating that there is no specific reason given, and combined with the unnecessarily long symmetric 16-mer barcodes, and 5’-block (5’ NH4-C6), they are pushing up the cost for little transparently good reason. Perhaps I am wrong. Any offered reasoning on these points would be appreciated.

I am at the same stage as you right now. I am assuming that you are planning a 2-step amplification: first one with the universal primer and second one with the barcoded primers. So, this has been my rationale and experience on this.
HPLC purification
If you are generating your own primers and not buying the plate from PacBio it is better to get HPLC purified oligos. The idea behind using HPLC purified primers is that the oligo synthesis may produce truncated products (primers with deletions usually towards the 5' region) in little concentrations. According to IDT, each base addition has an approximate error rate of 1%.  Therefore, longer products have a higher probability of deletions; the number of expected errors would be 0.01 × length of the primer. For a 46nt primer (16nt barcode + 30nt universal sequence), the percentage of deletion-free products would be ~63% (Poisson probability of no deletions). So, you can expect 27% truncated products with approximately 1.2 deletions per product†. Therefore there is some likelihood that the truncated products may mess up your barcode. However, the probability of the deletions specifically in the barcode regions would be less than this estimate.
5' NH4-C6 modification
This modification makes prevents the ligation of the PCR products. You generate the final library by re-amplifying the PCR products of universal primer, with the barcoded primers. The product will also contain a little amount of the template, which you do not want to be ligated to the sequencing adapters. Again, this would be very less: for example if you take 2ng of the template and your yield is ~1.5µg (I typically get this much yield even with a colony PCR of 25 cycles) then the template contamination is less than 0.2% (ideally you should calculate this with number of molecules instead of mass but since the template and product would have almost equal molecular weight you can use the latter also).
Why 16-mer barcodes
You can use shorter barcodes too but you should make sure that they are different enough such that any sequencing error would not make it difficult for you to distinguish between your barcodes. PacBio has an error rate of 13% for a single read; it reduces if you do the Circular Consensus Sequences (0.13^n where n is the number of rounds). When you have a large number of samples then it is better to use longer barcodes as you can reliably distinguish between different samples. They also recommend that the barcoded primers have a 5' phosphorylation. This will further increase your cost. The 5' phosphorylation will increase the ligation efficiency. It is technically possible to use polynucleotide kinase to phosphorylate the products but the efficiency of T4-PNK varies with the 5' base (Houten et al, 1998). In this case I would recommend pre-phosphorylated primers.
Why 30-mer universal primer
I don't have a good knowledge about this but I guess the reasons have to probably do with the molecular biology rather than the data analysis part of it. Demultiplexing can be done manually and it is not very difficult. Technically, a 20nt sequence should also suffice (usual length of PCR primers). Under usual circumstances, I don't think you are going to save a lot by using a 10nt smaller primer. The total length of primer (universal sequence + the template specific sequence) may go down from ~50+ to ~40+. Many oligo-synthesis services have an upper bound for HPLC purification; they would PAGE purify the longer ones. For example, the company that I order from has a cutoff of 50. So, longer primers have to be PAGE purified which would reduce your yield and increase the price. But usually you can negotiate with the company to allow your 1-5nt longer-than-cutoff product to be HPLC purified.

Summary
Some of these modifications would just improve the efficiency marginally and may be skipped if your data is not likely to be affected by a slight drop in efficiency.
So this is my final recommendation:

HPLC purification: not necessary but recommended for long primers (at least the barcodes)
NH4-C6 modification: not necessary
5' phosphorylation of barcoded primers: recommended
Length of universal primer sequence: can possibly be shortened by 10nt but probably that is not likely to reduce the cost significantly.

However, you can significantly reduce your cost by asymmetric barcoding. For example, if you have 100 samples then the minimum number of barcode primers needed would be 20 (10 pairs). You can shuffle the forward and reverse primers to create 100 combinations.

† Explanation of the error rate probability
Let $\lambda$ be the error rate per base (0.01) and $N$ be total number of bases (46). The error will follow Poisson distribution and the probability of errors would be:
$$P(X=k)=\frac{(\lambda N)^k e^{-\lambda N}}{k!}$$
For zero error i.e. $k=0$ the probability would be simply $e^{-\lambda N}$ which would be ~0.63
The mean number of deletions for the 27% that contain errors would be (see zero-truncated Poisson distribution):
$$E(X|X>0)=\frac{\lambda N}{1-e^{-\lambda N}} \approx 1.25$$

Thank you! I will accept and close this--great answer. But I should mention that I am still not clear on why 30-mer is necessary. I know it's proprietary, but the question is whether we can use something entirely different. The only reason for adhering to using a 30-mer is if the software that demultiplexes and removes primers must have the specified 30-mer. Else, I don't see why a shorter primer we designed (for 3'-RACE) would not perform better. I simply don't understand and cannot seem to find how this works in any of their many, many manuals. Anyway, it ought to be a separate question!

@Plantaloons I have edited my answer to discuss that point. However, it is still my guess and I can't say anything conclusively.

@Plantaloons I also have updated some of the calculations regarding HPLC purification.

What a terrific answer! Thank you very much.

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How are germ cells not reduced in number?
If germ cells produce haploid daughter cells by meiosis and are thereby "consumed" (where there was a germ cell there are then 4 daughter cells), where do the germ cells come from?  I asked my biology teacher if they undergo mitosis prior to meiosis, but she said they don't and proceeded to give an unclear answer.  Is this true?  If so, are they regenerated from somatic cells elsewhere in the body?
My question basically is - if the germ cells of, say, the testes are dividing by meiosis to produce sperm, where are the germ cells coming from so that the testes don't shrink and ultimately disappear as they're converted completely into sperm?

In case of gametogenesis (let us talk about spermatogenesis) gametes are formed from meiotic division of Primary spermatocytes.
In Primates Primary spermatocytes are cells that that are formed from mitotic division of B spermatogonia (which is another class of germ cells) which inturn are formed from mitosis of Ap spermatogonia which arise from mitotic division of Ad spermatogonia.  Ad spermatogonia are inturn formed from Primordial germ cells (see below for details).
Ad spermatogonia are dark A type spermatogonia, reserve stem cells  which occasionally divde to renew itself and Ap spermatogonia are pale A type spermatogonia, renewing stem cells.

Why the testis doesn't run out of germ cells? (adaptation of your key question)

The reserved  Ad spermatogonia and renewal of both  Ad and  Ap spermatogonia are responsible for the continuous cycles of spermatogenesis.

This process starts at puberty and usually continues uninterrupted until death, although a slight decrease can be discerned in the quantity of produced sperm with increase in age. (wikipedia)

The process of spermatogenesis in human:

In non-primates like mice it is little different, the following diagram should explain it:

Note:

Germ cells are cells that give rise to gametes ( present at any level of gametogenesis).
Primordial germ cells are embryonic cells that originate from a different location (outside the gonads) and migrate into the gonads during the course of embryonic development to divide into germ cells.
In females, oogenesis also involve production of germ cells (cells of primary follicles) from PGCs through mitosis but the primary follicles produced is fixed, doesn't increase after birth so at a definite age of 40-45 gametogenesis stops.

Further reading:

Stem Cells in Reproductive Medicine by  Carlos Simón, Antonio Pellicer, Renee Reijo Pera
A paper

Edited the answer making it specific to Primates which is relevant to your question. Thanks to @JayCkat.

"How are germ cells not reduced in number?"
It does happen. Germ cells do eventually run out. It is called menopause in women. And age related infertility in men.
As for your question of where do germ cell come from? Much like were do muscles cells come from?, you have to be specific. Germ cells comes from the gonads (ovaries and testis) would be a simple answer.
EDIT:

They are coming from Spermatogonial stem cells (SSCs), cells that for the most part are immortal, and can replicate endlessly (well ~60 years anyway).
https://www.ncbi.nlm.nih.gov/pubmed/23784829

any resources to add?


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What do we mean by distribution of species?
What is meant by distribution of species in the following context?

density-independent factors tend to limit the distribution of individuals and therefore of species.

I formatted your question, to improve readability.

From the limited context of the quote, it is referring to this definition of distribution (via Merriam-Webster):

a :  the position, arrangement, or frequency of occurrence (as of the members of a group) over an area or throughout a space or unit of time
b biology :  the natural geographic range of an organism

Or, if that isn't simple enough, it just means where the members of the species are located. In different contexts it may be simply the range, i.e., the space where any individuals of that species are located, or it might actually refer to the density as well.

Welcome to Biology.SE!

Species distribution is the manner in which a biological taxon is spatially arranged.

In the specific sentence you suggest, it seems that the term species range would have eventually be a little bit more appropriate though. The species range is the delimitation over space where individuals are found. The species range is just the maximum value in every possible direction of your species distribution.
Note however, that we often don't care too much about such semantic details (the sentence sounds correct to me).
Next time, please specify where you get the citation from 1) because context often matter and 2) because it is a copy right issue to not cite your source.

Same as above in simple terms
The term species distribution (and species range) describe the geographical locations of individual of the population (of a species). We are talking about a single species here. The term distribution takes the same definition than it does in statistics if you are used to it.
Imagine you have a population of oak trees. You can position every single individual tree over space Consider the drawing
Each individual is represented by a circle. The blue line represents a river.

Description of the species distribution: There are no individuals south east of the river. There is a clutch of high density at the north west of the study area.
Description of the species range is given by the red circle

The difference between species range and species distribution does not matter much for your purpose. The point is that you understand those terms are concepts describing the geographical locations of individual of the population (or the species if you prefer)

Hi can you please explain what that definition means using simple words ? My english is not good enough to understand that. By "species range" do you mean the amount of biodiversity within a particular species ? Or what ?

@Maxwhite Does that help?


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Rock cod vs grouper
What is the difference between a rock cod and a grouper? The only difference I notice is that grouper seems to be bigger in size. But other than that, they are very similar.

Added wiki links to your post. Adding links to content improve readability for curious and/or competent users, experts and those reviewing your posts.

I do not understand your question. They are phylogenetically speaking very far apart. The only thing they have in common is that they are ray-finned fishes, just like approx. 30000 other fishes.

The rock cods and the Groupers may look similar, but they belong to different "orders" and "families". Moreover here are the differences I mentioned:

ROCK COD

Kingdom:    Animalia
Phylum: Chordata
Class:  Actinopterygii
Order:  Gadiformes
Family: Moridae
Genus:  Lotella
Species:    L. rhacina

GROUPERS

Kingdom:    Animalia
Phylum: Chordata
Class:  Actinopterygii
Order:  Perciformes
Family: Serranidae
I have strong-texted the two differences. You also wrote that besides they look very similar, the Grouper family is slightly bigger in size than the cods. Well, you observation is correct, because the groupers are closely related with sea basses. In fact, sea basses are included to the same family like groupers: The Serranidae. The enlarged size of the groupers is because they have a degree of relativity with basses that as wikipedia says: Bass is a name shared by many species of fish. The term encompasses both freshwater and marine species, all belonging to the large order Perciformes, or perch-like fishes.
This justifies the size and big body weights we notice to the family serranids, like the common grouper.

This answer is adequate as it stands but could be made stronger by adding a simple phylogenetic tree and possibly a summary of key ecological niche differences.


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Hardy Weinberg principle
The principle is that sum total of all allelic frequencies is 1.
Individual frequencies for example can be named p,q.In a diploid cell , p and q represent the frequency of allele A and a respectively . The frequency of AA individuals in a population is p2  as the probability of an allele A with a frequency of p appear on both the chromosomes of a diploid individual is simply the product of the probabilities. Similarly for aa it will be q2.Can anybody explain that how it will be 2pq for Aa?
I am getting it as pq.

This question is really more about probabilities than H-W. Basically, you can arrive at Aa in two ways; either getting A from the father and a from the mother (Aa), or the opposite (aA). The probability of each combination of Aa is pq and the total probablility of both (Aa and aA) is therefore 2pq.

@fileunderwater: oops, my explanation might be super misleading. Thanks for clarifying!

@AlexDeLarge The binomial expansion that you gave (if I remeber correctly) is also correct to apply.

You almost said it all! Here are two ways to think of this problem
Finding the missing probability
Let's denote the fraction yz genotype in the population with $f(yz)$. The sum of of fraction of all genotypes must be equal to 1. In equation it means
$$f(aa) + f(aA) + f(AA) = 1$$
Here, of course I don't make a difference between $f(aA)$ and $f(Aa)$ (whether A is inherited from the mother or from the father). Knowing as you said
$$f(aa) = p^2$$
and
$$f(AA) = q^2$$
and feeding this value back to the first equation result into
$$p^2 + f(aA) + q^2 = 1$$
Solving for $f(aA)$ yields to
$$f(aA) = 2pq$$
Directly calculate the probability
Another to reach this result is to ask the following questions

What is the probability that the maternal allele is A?

The answer is $q$

What is the probability that the paternal allele is a?

The answer is $p$

What is the probability that the maternal allele is a?

The answer is $p$

What is the probability that the paternal allele is A?

The answer is $p$
Therefore, $$f(aA) = pq + pq = 2pq$$


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Scientific name of a certain plant from Philippines

Can someone tell me what is the possible scientific name of this plant? The seller told me it was sun rise plant but I can't seem to find it in the internet.
Location: Santa Rosa Laguna, Philippines

Please add a location to help us know where in the world you got it

Santa Rosa Laguna, Philippines


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What is this little white creature?
Please identify this little and soft white creature. Since childhood I am seeing this things flying in my surroundings and nowadays they are seen occasionally.

it's a seed - similar to dandelion, many species use wind dispersal

It's indeed a seed. It could help if you mentioned the geographical origin of the seed, but it could help even more if you could trace it back to its source plant.

It is, as stated by @rg255 a seed (or actually a fruit, see below). The seed itself is the small brownish thing. The white hairs are attached to make the seed fly with the wind. Looking at the seed and the hairs, I think the seed belongs to the daisy and dandelion familie asteracae/compositae. Altough there are other possibilities, see comments.
EDIT:
@AlwaysConfused is right if he states that in case of daisy family, it should be called a fruit, that containes one single seed. To be more precise, it is an Achene/Cypsula. In many species, what is often referred to as the "seed" is actually a fruit containing the seed. The seed-like appearance is owed to the hardening of the wall of the seed-vessel, which encloses the solitary seed so closely as to seem like an outer coat. Info derived from here on fruits and seeds and more specifically on Achenes/Cypsela here


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What species is this bird?
This bird is a frequent "visitor" at a lake south west of Berlin, GERMANY.

For more pictures here's a link:
https://goo.gl/photos/ADVSZwbDQUpbomCBA

It's a BLACK KITE (Milvus migrans). I bet you took the pics this summer because the great majority of the population is in Africa at the moment.
It is a black kite because:

rather uniform dark brown color
squared tail (it form a shallow v during gliding)
uniform underwing color and lighter head is a shared with marsh harrier but the absence of darker patch around the eye, the dark shoulder and 6 digitated primaries assure us is a black kite.

Here is a picture for reference:


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Do the activity patterns of an owl species determine their eye colour?
Recently I've been thinking about the colour of owl eyes, and trying to figure out if there is a pattern anywhere between species.
I have read for example, that yellow-eyes implies they are day time hunters.
Is this true, and if so what do other owl eye colours indicate about their behaviour?

No, there isn't a perfect link between eye colour and behaviour
The full claim, as reproduced here is as follows:

Yellow eyes point to day-active species, such as little owl.
Orange eyes indicate that the species is active at dusk and dawn, such as
long-eared owl (Asio otus).
Black eyes are for night-active species, such as tawny owl (Strix aluco).

However that same page also provides exceptions:

... a team of Spanish ornithologists gathered data on eye color and activity rhythm for over 200 owl species. The analyses revealed that dark irises were more frequent among strictly nocturnal owls (41 out of 70 nocturnal species) compared to owls that are active during or at the end of the day (37 out of 131 diurnal or crepuscular species). These numbers indicate that the statement from the television show was too general. There are plenty of exceptions to the rule. To name just two: the barn owl (Tyto alba) is diurnal and crepuscular but has pitch-black eyes. And the Sokoke scops owl (Otus ireneae) has bright eyes despite being active at night.

emphasis mine


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How do ants transport water?
All living things need water to survive. Worker ants can drink directly from the source. But a queen ant would need help from the colony to get its daily supply of food and water. I have seen ants carrying tiny bits of food, but I have not really seen them carrying water. Do they use their hands like how they carry food? Do they use a receptacle like us humans? Or are there some other innovative ways?

Ants are able to roll water droplets because of how small they themselves are in comparison. It seems odd but that's because different rules apply to the smaller creatures. For instance, a mouse falling from a skyscraper would be stunned, but otherwise uninjured. We, however, would break every bone in our body.

The worker ants give water to the other ants in the nest. Also, they get most of their hydration out of the food anyway.
Here is a blogpost with some references and nice humour about it.

The key word is trophallaxis.

Thank you. I love drinking water. so therefore I hate ants.


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Is better healthcare a bane to the long-term survival of the human race?
The theory of natural selection has it that individuals with better genes tend to survive and reproduce, passing their genes to their offspring. This gradual process results in a population more adapted at survival. However, due to the advancement in medical science, humans with poorer genes tend to survive and reproduce just as well.
For example, in the past, many people, excluding those with natural immunity due to some genetic mutations, would have succumbed to illnesses such as malaria and typhoid. But with better hygiene and medical treatment, these patients tend to survive.
Now, imagine a future where all illnesses including cancer can be treated. How would it impact the survival of the human race? Would we become more and more vulnerable such that our survival hinges heavily on medical technology, analogous to how an astronaut's survival is dependent on his spacesuit?

First, healthcare after reproductive age should not affect the survival of the humans as species. Second, if healthcare is here to stay, not just some temporary episode, then even healthcare for those under reproductive age shall not harm survival of humans, no more than knives and fire would harm survival. Think of healthcare as another tool like fire and knives and there should be no reason it would harm the survival.

Gene frequencies (frequencies of each allele at a given loci) in populations are affected by many things divided in to systematic and dispersive processes. Systematic process (migration, mutation, selection) affect gene frequencies in an often quite predictable manner and strength. Dispersive process (Random drift, differentiation between sub-populations, uniformity within sub-populations, increased homozygosity) are random in their direction and only predictable in their amount. Your question focusses on the systematic process called selection.
In a large population (if we ignore dispersive processes for the time being) the gene frequencies will reach an equilibrium called Hardy-Weinberg equilibrium. This means, with constant rates of the systematic processes, each locus will reach a point of stable equilibrium. Mutation and migration bringing more variation, and selection reduces it (over simplified - sometimes selection maintains variation, see my answer about why variation exists here). The frequency of each allele at equilibrium will be where these effects balance out. If selection becomes weaker against one allele it will become more frequent in the population.
By using medicine etc. to cure diseases we reduce the selection acting on a deleterious mutation thereby putting the gene frequencies in to a state of flux during which they move to new equilibrium points. So in short the answer is yes, modern medicine is decreasing our genetic fitness by allowing deleterious mutations to become more common.
I raise the question, will we ever be able to cure all genetically caused disease? In my reckoning, no, at least certainly not in our lifetimes.
It only represents a real risk if we suddenly are unable to cure diseases. This would increase selection against that allele and the gene frequencies would move back towards the equilibrium point which existed before the selection was reduced. What this means for the population is the loss (death) of those with the low fitness genotype.
The best reading you can do on this is the opening chapters of Falconer and Mackay's Introduction to Quantitative Genetics. Also read about Hardy-Weinberg equations.
HTH

I have to read a few times to understand. But this is certainly a great answer!

I know how you feel, I have read the chapters in that book many times and they are not easy! condensing it down was hard!

"It only represents a real risk if we suddenly are unable to cure diseases." True that. -- Late to the party but have you considered that one possibility is the degradation of our ability to think well? The only realistic (and hopefully astronomically unlikely) scenario in this regard is where humanity is dependent on technology and the tech fails for some reason. -- Biological warfare seems orders of magnitude more likely to cause us serious permanent harm .

The theory of natural selection has it that individuals with better genes tend to survive and reproduce, passing their genes to their offspring.

Yes, under selective pressure, that is. The stronger the selective pressure, the more the population will change. Without a selective pressure, there isn't an impetus to change.

However, due to the advancement in medical science, humans with poorer genes tend to survive and reproduce just as well.

You're making a mistake. "Poor" and "Good" are purely contextual. You might say that Sickle Cell Anemia is a poor lot to be stuck with... Unless, of course, you're in an area ravaged by Malaria. Then it's a boon.
What would be more accurate is that there aren't any strong forces acting upon humans that causes selective pressure and the proceeding adaptation. Of course, we are the result of such evolution, so by a basic standard all modern humans who reproduce are fit in a Biological sense.

For example, in the past, many people, excluding those with natural immunity due to some genetic mutations, would have succumbed to illnesses such as malaria and typhoid. But with better hygiene and medical treatment, these patients tend to survive.

The brain is the one of the finest products of evolution. Because we're no longer dying en masse at the whims of bacteria or virii (usually) does not mean we haven't adapted. Our ability to build advanced tools and perform science is an adaptation. One for which we pay heavily; we're practically helpless until our teens.

Now, imagine a future where all illnesses including cancer can be treated. How would it impact the survival of the human race?

We'd live longer, and assuming the rate of reproduction stays the same, there'd be a lot more of us.

Would we become more and more vulnerable such that our survival hinges heavily on medical technology, analogous to how an astronaut's survival is dependent on his spacesuit?

Well... Vulnerable to what? To disease? Probably not. Current Immunizations and treatments often utilize the body's own immune system; basically getting sick and all the benefits of encountering the disease without the side-effects of significant death.
To genetic diseases? No. The human population has exploded in the last hundred or so years, and our genetic diversity has been greater than at any point in the last 40,000 years when a major bottlenecking event occurred. For a genetic disease to deal significant damage on a species, it would have to be suffuse throughout the population. That's not happening.
To a post-apocalyptic world where technology breaks down and suddenly we're facing off against parasites and predators? Well, if the event ever occurs, then a lot of us won't be ready, that's for sure. The stress such a life put on us in the past limited our lifespan to nearly half what it is now, but unless there's a complete lack of knowledge many basic safety habits should persist. Cooking, boiling water, dressing wounds, how illnesses spread - these are all things which dramatically increase quality of life when utilized correctly.
Will we ever reach a point where we, quite literally, cannot live without technological intervention? No idea. Humans have very, very strong reactions to things which aren't human but appear human (The Uncanny Valley is a great example). It's just as possible that those instincts will prevent us from such a fate as the possibility that we'll be completely fine with becoming cyborgs. Nobody can even begin to give you a time-frame, though. As-is, there's no reason to become cyborgs (no Selective Pressure), and won't be for the foreseeable future.


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How do parasitic fungi sense optimal fruiting conditions from inside the host?
Question is pretty straight forward. Are there generally any chemical cues?

In model fungi, the G protein coupled receptor Gpr1 is known to sense sugars and upregulate a cAMP linked PKA pathway, while in pathogenic strains, it senses Methionine. This probably is the environmental cue that sets off fruiting. There is a recently published extensive review too: Heterotrimeric G protein signaling in filamentous fungi

Reference

Li, Liande, Sara J. Wright, Svetlana Krystofova, Gyungsoon Park, and Katherine A. Borkovich. “Heterotrimeric G Protein Signaling in Filamentous Fungi.” Annual Review of Microbiology 61, no. 1 (October 2007): 423–452.


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Identifying this spider
I think this is a spider. 8 legs, 2 body sections, and 2 really long Palos? Anyways, can anyone identify this bug, or point me to a resource where I could classify it?

Welcome to Biology.SE! Please include your location and an approximate size of the species. And also add multiple close-up images from different sides. See here for more information

It's camel spider, they have large pedipalps, big chelicerae, and their body is covered by little "hairs". As far as I know, there are only 2 families of that order in North America

Welcome to Biology.SE! Please add some more details and references to your answer, along with some images for comparison.

Some spider species are easy to identify as they're relatively common and well-known or though less common, have unusual or distinctive enough markings/coloration, they won't generally be mis-identified.
Since you live in the US, the species will be better identified by another American rather than someone from other another continent. Bug Guide (hosted by the Department of Entomology at Iowa State University) has an ID Request page where images can be posted and amateur and professional experts will look at and identify. You need to register but it's free. The clearer and more detailed your photo(s), the faster it'll be viewed and answered.
It's worth joining. There's a lot to learn and you may find learning about 'bugs' addictive with no bad effects?

I hardly think my answer warranted a downvote. Not living in the US, I didn't recognise it. The OP did ask for identification OR to be pointed to a resource that could help. BugGuide is an excellent resource for identifying arthropods.

I agree with @Jude: downvote might be justified if there was something misleading identification in the answer, but here there is no identification attempt. One could argue that this could have more typically been a comment rather than an answer, but given the fact that the original poster requested for identification resources, this may qualify as an answer.


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help identify this fish

I came across this washed up fish in Panama City, Florida in November 2015. I'm guessing it's a puffer fish but I can't find anything like it online.
Thanks.

Search "boxfish". I see several in my ID book that look like contenders. I haven't seen this one in the wild so, lacking other viewing angles, that's as close as I gain get.

For real, this fish has a pattern of perfect hexagons? How cool is that!

This is a kind of trunkfish. (They have different names, this could be a smooth or spotted trunkfish.). It's really a lovely and comical little fish when observed alive in coral reefs. It has the ability to change its coloration depending on whether it's excited or calm, or to minimize its contrast to the background. It is related to puffer fish.
It has a boxy, triangular body shape, and propels itself with relatively tiny, delicate fins. Like pufferfish, they are toxin producers.

In death, the body shape and coloration are different, of course. Never saw a dead one before; sad. The juveniles are adorable:

Members of this family occur in a variety of different colors, and are notable for the hexagonal or "honeycomb" patterns on their skin. - Wikipedia

Trunkfish it is. Thanks for the help. It was around 12" in length, beautiful fish. I thought the pattern was too cool.

@Thomas - The pattern is really incredible; you can see it go from dark with spots to light with marked hexagons. Amazing fish, one of my favorites when diving. And because they are toxic and have few predators, they are not very shy at all.


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Why is black and yellow such a nice camouflage?
Many people can`t differenciate between cheetahs, leopards and jaguars, but there are serveral other animals with a similar pigmentation (servals, ocelots...), why is it so effective? It gets exciting when you realize that cheetahs and leopards are evolutionaray relatively far away, and therefore that their resemblance exsists due to evolutionary convergence.

What makes a camouflage effective? It has to match the colors and color patterns of the habitat.
Here are two cheetahs

Here is another cheetah

Here is a leopard

Here is a jaguar

Overall, it looks like their yellow and black pattern is a pretty good camouflage.
The jaguar habitat is a mixture of open and forested habitats. One would think, the jaguar would gain by being a little greener but there is a good reason for the jaguar not being green (see Why is green fur not a thing?).
Note also that it would be a mistake to think that any species should be perfectly adapted to its environment. You might want to have a look at the paragraph Did you say Natural Selection? in this answer for a very short intro to why populations might sometimes be less adapted than a naive observer may expect. There might have an important phylogenetic signal among these felidae (you might to have a look at the paragraph Why 4 legs? in the same answer as indicated above).


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Please identify this bug/insect
Ten of these bugs were found behind my bed. I live in Northern California.
The bug is 5mm in length.

It seems to me a kind of larva.

I think you are correct. After doing a web search, I believe it is carpet beetle larva. Here is a link: http://www.bugzapperpestcontrol.com/blog/wp-content/uploads/2016/05/Varied-Carpet-Beetle-Larva.jpg

Sure looks like the picture. If your room is carpeted and the carpet is edible, e.g. wool versus a total synthetic, that might offer some conformation.

Thank you all for your help.  I will mark it as a duplicate as per rg255's suggestion. My room is fortunately not carpeted, but I had some old rope behind my bed, and I think they were eating that.

Carpet beetle larvae  feed on basically any organic matter... Also, yes, this is definitely a carrpet beetle larvae


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Human anti animal antibodies issues in blood testing
Do people have to be exposed to animals to get HAMA antibodies? Can these antibodies impact blood tests with false negatives as well as false positives?

Hi Chris, totally understand, my apologies. I have reworded the question to gain some more clarity on the topic in general.

You do not need to be exposed directly to animals to get human anti-mouse (or human anti-animal) antibodies; you can also be exposed to animal products in various ways.

Circulating anti-animal antibodies can arise from iatrogenic and noniatrogenic causes. The former is the result of the normal response of the human immune system to an administered “foreign” protein antigen. Currently available diagnostic and pharmaceutical agents derived from an animal source are extensive and range from rodent immunoglobulins to hormones isolated from fish. In addition, some recombinant proteins are affinity purified on immobilized monoclonal mouse antibody columns, and the possibility exists for some of the mouse monoclonal antibody to detach and copurify with the protein

You can also get anti-animal antibodies from blood transfusions:

Blood transfusion is also associated with an increased incidence of anti-animal antibodies. A study of 2829 participants in a population health survey revealed that 14.4% of the participants who had been transfused were anti-animal positive, compared with 10.4% of the participants who had never received a blood transfusion. This difference was presumably attributable to infusion of preexisting human anti-animal antibody or as a result of infusion of a foreign antigen present in the unit of blood

or through vaccination:

Vaccination against infectious diseases is another route by which animal protein antigens may be inadvertently presented to the immune system and trigger antibody formation. In the US, chick embryo or egg cultures are frequently used in vaccine production, and residual chicken protein may be present in vaccines, whereas in Europe, some vaccines contain rabbit serum, e.g., rubella vaccine in France, and multimicrobial vaccine (Bruschettini vaccine) in Italy

or "unconventional therapies":

The administration of unconventional therapies is also a route to immunization with animal protein. For example, a patient developed anti-rabbit antibodies following injections of “antireticulocytoxique”, which is a lyophilized serum obtained from rabbits injected with homogenates of human bone marrow and spleen and is intended as a tonic to improve senescence and to reduce fatigue and debilitation

Other routes:

Noniatrogenic causes of anti-animal antibodies include maternal transfer across the placenta to the unborn child (37)(38), animal husbandry or the keeping of animals as pets (39), and the transfer of dietary antigens across the gut wall in conditions such as celiac disease (40)(41). Anti-animal antibodies are also more common in multiparous females (36), and a high incidence of human anti-animal antibodies has also been observed in association with certain disease states, e.g., idiopathic cardiomyopathy

All quotes from Human Anti-Animal Antibody Interferences in Immunological Assays, by Larry J. Kricka (1999).

fantastic answer. Thank you for being so comprehensive.


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Why do most organisms have negative supercoiled DNA?
It has been observed that in nature most organisms have negative supercoiled DNA and that few organisms have positive supercoiled DNA. Some of the organisms that have the positive supercoiled DNA live in strong acidic environments but are very rare compared to negative supercoiled DNA. Why wouldn't all organisms have the same DNA supercoiling? Does it affect their survival in any way?

Very briefly, positive supercoiling can help prevent DNA denaturation. It's sometimes (often?) found in thermopiles since their DNA is prone to melting.

Negative supercoiling reduces the torsional energy. Positive supercoil is like a compressed spring.

@WYSIWYG It sounds like that could be an answer if its explained why that matters?

One important notion in DNA topology is the linking number ($Lk$) which is the sum of right-handed twisting # and left-handed writhing # ($Tw+Wr$). Say the $Lk = x$ for relaxed DNA. If $Lk<x$ then you have negative supercoiling while positive supercoiling happens when $Lk>x$.
The higher the $Lk$ value the higher the helical energy of the DNA and the harder it is to separate it meaning the DNA is now more stable. In so-called "extreme" conditions (e.g. high acidity or high T˚) the organism must protect his DNA from degradation. Therefore those organisms require a more stable form of their DNA which can be achieve by positive-supercoiling and/or high GC content.
Now why do the vast majority of the organisms have negatively-supercoiled DNAs? If you let the DNA by itself, it will adopt an $Lk=x$, i.e. it will be in his "relaxed"-form. Negative supercoiling arose because of the presence of Topoisomerases (type I and II), which are proteins that cleave the DNA and release the helical tensions and which cumulatively provokes the DNA to be slightly underwinded compared to it's relax-form. Is this good for the organism, if living in non aggressive conditions? Yes it is because a decrease of the $Lk$ will make the DNA easier to separate. This means replication and transcription can occur more easily or in proper terms, they now require less energy to perform their functions.
Here an excellent reference on this subject as well as a Youtube video that explains those concepts using strings. The latter is really helpful as those concepts are easier to understand visually than in writing.
I hope this helps.

in negative super coiling  number of the times the strands cross each other is LESS than positive super coiling making it easier to unwind it for the processes of replication,transcription....


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I just saw this bird outside my apartment. Anyone know what it is? (Texas, US)
Saw this bird outside my apartment in College Station, Texas  and have never seen anything like it before!
It is about the size of a hand.

Nice camouflage and funny tail.

That species is so... special. Unique, beautiful and contrasting, all in one.

It's also worth noting that these birds are the subject of some wonderful youtube videos

It is American Woodcock, Scolopax minor.

Superbly camouflaged against the leaf litter, the brown-mottled American Woodcock walks slowly along the forest floor, probing the soil with its long bill in search of earthworms. Unlike its coastal relatives, this plump little shorebird lives in young forests and shrubby old fields across eastern North America. Its cryptic plumage and low-profile behavior make it hard to find except in the springtime at dawn or dusk, when the males show off for females by giving loud, nasal peent calls and performing dazzling aerial displays.

The newborns are even more camouflaged in downs.
References:

Audubon
All about birds

I've found whatbird.com to be pretty good for identifying American birds.  Asking it for grey and brown medium-sized birds that are commonly found in Texas gives 14 options, of which the best match is the American woodcock, as suggested by Sanjukta (which is conveniently early on the alphabetical list!)


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Identify this spider from Bangladesh
Location: Jahangirnagar university, Savar, Bangladesh

EDIT: Here is the video from which image is taken

It  is a jumping spider. Could be Genus Epocilla sp. .
Jumping spiders have their posterior lateral eyes placed high up the cephalothorax and the rest three pairs in a typical arrangement as observed in your specimen.

An image of Epocilla sp. from Wikipedia.
Your specimen more closely resembles the E. calcarata .

Epocilla calcarata? http://farm2.static.flickr.com/1265/1229102333_2d73378d43.jpg

I can't assure. Not an Arachnologist myself, I think an expert can shade some light.

Accurate Spider identification to species level is done by viewing the tiny structures of their anatomy under a microscope examining the spider’s reproductive organs. To find out which family your spider belongs to comes with experience. Helpful in identification are the eyes of the spider and they are not visible in this photograph. How many does it have? How are they arranged? How does each eye’s size compare to those around it? Here is a helpful link to some rules for identification. Good luck!!
http://www.spiders.us/articles/identification/#spider-location

Here is a video. https://youtu.be/52lSx_yl45A

Welcome to Biology.SE. Your answer seems more like a comment and does not fit our standards for good answers (see here and take the tour) - this is not a common discussion forum, so if you cannot answer the question, you should not give an answer. As is, your answer is very likely to be down-voted or deleted. Please edit you question if you want to make a suggestion regarding the id of the spider or delete it if you do not have a suggestion. Thank you!


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How could humans have interbred with Neanderthals if we're a different species?
To be clear, I'm not doubting that Homo sapiens and Homo neanderthalensis did interbreed: of that much I'm convinced.
Within the past few years I've seen an upcropping of pop-sci articles discussing the interbreeding between pre-historic species of humans. In everything that I see in these articles, as well as in scientific literature (my college Bio textbook, among others), I see these different human groups being referred to as separate species.
This conflicts with my understanding of a species. Given the following definition, wouldn't Homo sapiens and Homo neanderthalensis be the same species?

A species is often defined as the largest group of organisms where
two hybrids are capable of reproducing fertile offspring, typically
using sexual reproduction.  ~Wikipedia

Is this definition incorrect?
Are the publications using "species" colloquially, as opposed to scientifically?
Is "species" still a poorly defined concept? (see Ring Species)

Thanks!

Short answer
The concept of species is poorly defined and is often misleading. The concepts of lineage and clade / monophyletic group are much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.
Note that Homo neanderthalis is sometimes (although it is rare) called H. sapiens neanderthalis though highlighting that some would consider neanderthals and modern humans as being part of the same species.
Long answer
Are neanderthals and modern humans really considered different species?
Often, yes they are considered as different species, neanderthals being called Homo neanderthalis and modern humans are being called Homo sapiens. However, some authors prefer to call neanderthals Homo sapiens neanderthalis and modern humans Homo sapiens sapiens, putting both lineages in the same species (but different subspecies).
How common were interbreeding between H. sapiens and H. neanderthalis
Please, have a look at @iayork's answer.
The rest of the post is here to highlight that whether you consider H. sapiens and H. neanderthalis to be the same species or not is mainly a matter of personal preference given that the concept of species is mainly arbitrary.
Short history of the concept of species
To my knowledge, the concept of species has first been used in the antiquity. At this time, most people viewed species as fixed entities, unable to change through time and without within-population variance (see Aristotle and Plato's thoughts). For some reason, we stuck to this concept even though it sometimes appears to not be very useful.
Charles Darwin already understood that as he says in On the Origin of Species (see here)

Certainly no clear line of demarcation has as yet been drawn between species and sub-species- that is, the forms which in the opinion of some naturalists come very near to, but do not quite arrive at the rank of species; or, again, between sub-species and well-marked varieties, or between lesser varieties and individual differences. These differences blend into each other in an insensible series; and a series impresses the mind with the idea of an actual passage.

You might also want to have a look at the post Why are there species instead of a continuum of various animals?
Several definitions of species
There are several definitions of species that yield me once again to argue that we should rather forget about this concept and just use the term lineage and use an accurate description of the reproductive barriers or genetic/functional divergence between lineage rather than using this made-up word that is "species".
I will below discuss the most commonly used definition (the one you cite) that is called the Biological species concept.
Problems with the definition you cite

A species is often defined as the largest group of organisms where two hybrids are capable of reproducing fertile offspring, typically using sexual reproduction.

Only applies to species that reproduce sexually
Of course, this definition only applies to lineages that use sexual reproduction. If we were to use this definition for asexual lineages, then every single individual would be its own species.
In practice
In general, everybody refers to this definition when talking about sexual lineages but IMO few people are correctly applying for practical reasons of communicating effectively.
How low the fitness of the hybrids need to be?
One has to arbitrarily define a limit of the minimal fitness (or maximal outbreeding depression) to get an accurate definition. Such boundary can be defined in absolute terms or in relative terms (relative to the fitness of the "parent lineages"). If, the hybrid has a fitness that is 100 times lower than any of the two parent lineages, then would you consider the two parent lineages to belong to the same species?
Type of reproductive isolation
We generally categorize the types of reproductive isolation into post-zygotic and pre-zygotic reproductive isolation (see wiki). There is a lot to say on this subject but let's just focus on two interesting hypothetical cases:

Let's consider two lineages of birds. One lineage has blue feathers while the other has red feathers. They absolutely never interbreed because the blue birds don't like the red and the red birds don't like the blue. But if you artificially fuse their gametes, then you get a viable and fertile offspring. Are they of the same species?

Let's imagine we have two lineages of mosquitoes living in the same geographic region. One flying between 6 pm and 8 pm while the other is flying between 1 am and 3 am. They never see each other. But if they were to meet while flying they would mate together and have viable and fertile offsprings. Are they of the same species?

Under what condition is the hybrids survival and fertility measured
Modern biology can do great stuff! Does it count if the hybrid can't develop in the mother's uterus (let's assume we are talking about mammals) but can develop in some other environment and then become a healthy adult?
Ring species in space
As you said in your question, ring species is another good example as to why the concept of species is not very helpful (see the post Transitivity of Species Definitions). Ensatina eschscholtzii (a salamander; see DeVitt et al. 2011 and other articles from the same group) is a classic example of ring species.
Species transition through time
Many modern lineages cannot interbreed with their ancestors. So, then people might be asking, when exactly did the species change occurred? What generation of parent where part of species A and offspring where part of species B. Of course, there is no such clearly defined time in which transition occurred. It is more a smooth transition from being clearly reproductively isolated (if they were placed to each other) from being clearly the same species.
Practical issue - Renaming lineages
How boring it would be if every time we discover the two species can in some circumstances interbreed, we had to rename them! That would be a mess.
Time
Of course, when we talk about a species we refer to a group of individuals at a given time. However, we don't want to rename the group of individuals of interest every time a single individual die and get born. This notion yield to the question of how long in time can a single species exist. Consider a lineage that has not split for 60,000 years. Was the population 60,000 years ago the same species as the one today? The two groups may differ a lot phenotypically and may actually be reproductively isolated if they were to exist at the same time.
Special cases
When considering a few special cases, the concept of species become even harder to apply.
The Amazon molly (a fish) is a "species" that have "sexual intercourse" without having "sexual reproduction" and there are no males in the species! How is it possible? The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used (Kokko et al. (2008)).
In an ant "species", males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) and don't need each other to reproduce. In this respect, males could actually be called females. But they still meet to reproduce together. The offsprings of a male and a female (via sexual reproduction) are sterile workers. So males and females are just like two sister species that reproduce sexually to create a sterile army to protect and feed them (Fournier et al. (2005)).
Bias
It often brings fame to discover a large new species. In consequence, scientists might tend to apply a definition of species that allow them to tell that their species is a new one. A typical example of such eventual bias concern dinosaurs where many new fossils are abusively called a new species while they sometimes are just the same species but at a different stage of development (according to this TED).
So why do we still use the concept of species?
Naming
IMO, its only usefulness is that it allows us to name lineages. And it is very important that we have the appropriate vocabulary to name different lineages even if this brings us to make a few mistakes and use some bad definitions.
The alternative use of the concept of lineage
It is important though that we are aware that the concept of species is poorly defined and that if we need to be accurate that we can talk in terms of lineages. The main issue with the term lineage is not semantic and comes about the fact that gene lineages may well differ considerably from what one would consider being the "species lineage" as defined by the "lineages of most sequences"... but this is a story for another time.
In consequence
In consequence to the above issues, we often call two lineages that can interbreed to some extent by different species names. On the other hand, two lineages that can hardly interbreed are sometimes called by the same species name but I would expect this case to be rarer (as discussed by @DarrelHoffman and @AMR in the comments).
Homo lineages
I hope it makes sense from the above that the question is really not related to the special case of the interbreeding between the Homo sapiens and the Homo neanderthalis lineages. The issue is a matter of the definition of species.
Video and podcast
SciShow made a video on the subject: What Makes a Species a Species?
For the French speakers, you will find an interesting (one hour long) podcast on the consequence of the false belief that the concept of species is an objective concept on conservation science at podcast.unil.ch > La biodiversité - plus qu'une simple question de conservation > Pierre-Henry Gouyon

Here is a related answer

Might also be worth mentioning the flip-side of this, that just because two animals are considered the same species does not guarantee they are capable of producing offspring.  For example, all domestic dogs are generally considered a single species, but a female Chihuahua would be unlikely to be able to produce a viable litter with a male Great Dane.

@DarrelHoffman however a female Great Dane could produce a litter with a  male Chihuahua. On a chromosomal level, they are pretty much the same. Pure bred French Bulldogs have to be delivered via Caesarean, as even the females of the breed are not able to birth the heads of their offspring.

In reaction to your comments I added two sections: In consequence and The bias of Humans. Let me know if this seems good enough and whether I should develop it further. Thanks

Although the discussion on problems with the species concept is interesting, I find this answer to be quite strongly worded/controversial (against "species", for "lineages"), but still basically lacking references (except a couple of tangential links). I would like to see a clearer separation between personal opinion and scientific consensus and/or ongoing scientific discussions.

@fileunderwater I agree with you! I have discussed a good part of these ideas with colleagues and also with Pierre-Henri Gouyon after a talk he made about the detrimental effect of the concept of species in conservation biology. If you speak french, you can find a podcast here under "La biodiversité - plus qu'une simple question de conservation" Sorry, I can't cite any papers.

Given the inherent subjectivity of the terminology surrounding species, do you think it's feasible to use the concepts of lineage and/or clade in everyday conversation in the same way that species is? I frequently have discussions with my friends that would strongly benefit from more accurate language in reference to historical biological lineages, but actually using lineage in conversation has proven to be extremely complicated compared to the more inaccurate species identifier. Is there a better way?

The definition of species is open for debate, and this is especially the case when you try to define it from a paleontology perspective.
Homo neanderthalensis was first discovered and defined in the 1860's, long before we were able to sequence their genome, which was published in 2010. There genome was different enough that most scientists would still say that they are distinct from modern humans, but that doesn't necessarily mean that those distinctions were enough that it affected the ability to produce fertile offspring between sapiens/neanderthalensis matings.
In fact on the wikipedia article I linked to the alternative Homo sapiens neanderthalensis is suggested as a synonym making us Homo sapiens sapiens for anatomically modern humans. This is similar to distinctions made in the wolf lineages where you have Canis lupus for grey wolves, Canis lupus familiaris for Domestic dogs, Canis lupus dingo for the wild dogs of Australia, and on and on for many other sub species of Canis lupus. Wolf/Dog hybrids are known to be fertile.
Female Horses and Male Donkeys can breed to create sterile offspring, Mules. The sterility is likely due to the fact that there is a greater phylogenetic distance between Horses and Donkey than there is for sapiens/neanderthalensis and also due to the fact that Horses have a different number of chromosomes to Donkey's , where as sapiens/neanderthalensis have the same number.
Another thing you have to remember is that the discovery of Homo neanderthalensis occurred about 5 years after Darwin created an uproar about Humans being evolved primates. Now you were faced with a skeleton that clearly was different from modern human but was clearly hominid. The closely held view that humans were special and therefore held dominion over all other creatures made it difficult to accept the fact that we may actually have evolved.

I am confused by your last paragraph. Was Homo neanderthalensis not regarded as part of human evolution?

@CarstenS, the paragraph might be confusing if one does not realize that Darwin's evolutionary ideas at the time met much cultural resistance since it seemed to be in conflict with the idea that man was specially created to have dominion over the world.

In addition to @Remi.b's answer on the species concept, and the perils of using human definitions to try to encompass biological reality, you need to understand what "interbreeding" meant to humans and neanderthals.  Fertile crosses between sapiens and neandertalis were very rare, probably less than one successful cross per generation, and there's some evidence that male hybrids were almost all sterile (or that this was a fatal condition).  This is probably less successful interbreeding than horse-donkey crosses, where the two partners are unambiguously different species by just about any definition (they have different chromosome numbers!).  So it's not like sapiens and neandertalis could effortlessly hybridize; it was very rare and generally unsuccessful.
References:

We find that observed low levels of Neanderthal ancestry in Eurasians are compatible with a very low rate of interbreeding (<2%), potentially attributable to a very strong avoidance of interspecific matings, a low fitness of hybrids, or both. These results suggesting the presence of very effective barriers to gene flow between the two species are robust to uncertainties about the exact demography of the Paleolithic populations, and they are also found to be compatible with the observed lack of mtDNA introgression. Our model additionally suggests that similarly low levels of introgression in Europe and Asia may result from distinct admixture events having occurred beyond the Middle East, after the split of Europeans and Asians.

--Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression. Currat M, Excoffier L. Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15129-34

Our results indicate that the amount of Neanderthal DNA in living non-Africans can be explained with maximum probability by the exchange of a single pair of individuals between the subpopulations at each 77 generations, but larger exchange frequencies are also allowed with sizeable probability.

--Extremely Rare Interbreeding Events Can Explain Neanderthal DNA in Living Humans. Neves AGM, Serva M PLoS ONE 2012 7(10): e47076

These results suggest that part of the explanation for genomic regions of reduced Neanderthal ancestry is Neanderthal alleles that caused decreased fertility in males when moved to a modern human genetic background.

--The genomic landscape of Neanderthal ancestry in present-day humans Sankararaman et al Nature 2014 507:354–357

"Fertile crosses between sapiens and neandertalis were very rare, probably less than one successful cross per generation, and there's some evidence that male hybrids were almost all sterile (or that this was a fatal condition" This is interesting. I would like to read more about it... could you provide references to this?

Among others - Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression. Currat M, Excoffier L. Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15129-34;
Neves AGM, Serva M (2012) Extremely Rare Interbreeding Events Can Explain Neanderthal DNA in Living Humans. PLoS ONE 7(10): e47076;
The genomic landscape of Neanderthal ancestry in present-day humans Sankararaman et al  Nature 507, 354–357 (2014)

Hi, I have one dumb question about this answer: why was human-neanderthal interbreeding probably less successful than horse-donkey crosses? Haven't horses and donkeys been crossed more often, with $0$ recorded instances of fertile offspring, while humans and neanderthals interbred less often, with nonzero instances of fertile offspring?

@Will - it's not true that there are no recorded instances of fertile donkey/horse offspring.  This article and this one list several well-documented examples in the past century, quite possibly more instances than all successful sapiens/neandertal crosses over the thousands of years they co-existed.

@iayork Oh cool I never knew about that, thanks! I guess to be fair though the descendants of human-neanderthal hybrids seem to have been able to make some contribution to the human gene pool, while even the rare fertile mules don't seem able to produce offspring capable of living long enough to contribute to either the donkey or horse gene pools. But I might be misunderstanding.

@Will Human/Neandertal hybrids almost certainly had some selective advantages that counterbalanced their strong disadvantages and led to some of the Neandertal genome being maintained -- speculation includes immunological advantages from Neandertal genes.  But also, it's likely that some Neandertal genes were carried along simply because of the general expansion of H. sapiens, even where those genes were neutral or even weakly harmful.

+1 for pointing the rareness of sapiens-neanderthal interbreeding. That is a very needed complement to the accepted answer since it seems to be misunderstood in the question.

The same way lions and tiger are different species but can interbreed. They do so poorly, not very often, and the male hybrids are infertile, although the female hybrids retain some fertility. Gene flow between the two species is possible but very limited. We call lions and tigers two species because gene flow between the two is limited. Free flow of genes between the two species is not possible.
If we look at the papers coming out it is obvious that the flow of genes between Homo Sapiens and Neanderthals was limited. It was so limited that we can say that two species were on the verge of cutting all ties between each other.
Firstly, there are no Neanderthal mitochrondria, meaning successful mating involving Neanderthals was mainly between human females and male Neanderthals. Next there are no Neanderthal Y chromosomes, meaning male hybrids were sterile.
Although there are Neanderthal gene in autosomes, there are no Neanderthal genes on X chromosomes, which house many of the genes regulating intelligence and fertility. So natural selection has selectively weeded out Neanderthal genes in those two areas, probably because they don't play well with their human counterparts (i.e. they cause a fitness disadvantage).
Also, the Neanderthal gene segments, although found in all non-Africans, are in small pieces. Individual have less than 2% (although as much as 35-60% of the Neanderthal genome remains in the non-African human population). So it means that the hybridization event occurred rarely and far in the past — probably when the first Homo sapiens left Africa.

There is a lot of conjecture in your answer and no evidence at all. Even though the notion of your answer might be correct, your conclusions are - given the data - way too strong and some of the information are even wrong (there is introgressed Neandertal DNA on the X, just about 5 times less then on autosomes). You will not find references to support most of your claims. -1

Really? I would think anybody would has read the literature would have said the same. All i am doing is repeating what has already been said. I am not adding anything new. Even my conclusion are just repeating the what has been concluded. The hottest thing is how many other species have been added to our genome. When and where. Latest news indicate that the how Neanderthal gene got into the human population is far more complicate that a single one off event.

No, you are putting it way too strongly. There is indicative evidence to support some of your claims, but nothing shows that the admixture events occurred only once or only far back in the past or even that male hybrids in fact were sterile. And just because we have not found Neandertal mitochondria or Y-chromosomes does not imply that there are none - absence of evidence is not evidence of absence. Remember that a mitochondrial genome is just one locus and how efficient drift is in populations with small effective sizes. The evidence is far from decisive.

A microbiology professor once told us "The Russians have about 14 times more species than the English"
The word species (Greek εἶδος¹) begins in greece. According to St. Thomas Aquinas (Summa Theologica, ca. 1265-1274 A.D.),  used as the scientific way of referring to different types of living things.
It's a notable buzzword in english owing to it's rhyming syllables, it focuses attention, and my... It isn't more precise than referring to colours... Espèces in French doesn't warrant the same obsessive buzz. Genetics is a spectrum and we divide them as best we can a bit like we divide colours of the rainbow.
Neanderthals came about only half a million years ago, and we diverge from them perhaps a million years ago.
Dinosaur species usually live for about 3 to 10 million years before changing two new species according to scientists, and their generations are closer together than humans...
So they are closer than bonobos and classical chimpanzees, perhaps something like the northern and the southern white rhino.

I'm not really educated into the scientific community's mindset very much, but as a person who is interested in taxonomy to one degree or another, as well as plant breeding, I can give you some perspective to help you decide on an answer.
Lots of different species can hybridize (interspecies hybrids): e.g. some different pepper species, some different tomato species, some different toad species, cows and bison, lions and tigers, different species of strawberries, etc. Interspecies hybrids sometimes even become invasive species. For instance, collared doves invaded my area years ago, and hybridized with the native doves (which native doves were quite a bit different: much smaller, much different behavior; they made different sounds, and had no collars); we've had the hybrids ever since (although they took some years to stabilize much--which was a fascinating process to observe), and the other two species appear to be gone, for the most part. In my personal opinion, interspecies hybrids (perhaps^ driven by changes in habitat: for instance, if the magnetic fields of the earth change, maybe because of a disturbance caused by a solar storm, animals might migrate different places than they used to, because some animals migrate via their ability to detect magnetic fields; if they migrate different places than usual, they might find new animals to hybridize with) are a very significant driver of new forms of life, which often gets overlooked.
^That's a hypothesis of mine, anyway. I don't claim it's a proven fact.
There are even hybrids between different genera, although they're pretty rare (sheep and goats have been known to cross, for instance; hybrids can also supposedly be made between goji and tomatoes--although I have yet to see plants or seeds of the hybrid for sale).
My impression from things I've studied isn't that species differentiate sexually incompatible groups, but rather that they differentiate sexually compatible groups that tend to stick together. (You're probably not going to see llamas and camels hanging out very often, or horses and zebras, or donkeys and zebras, but that doesn't mean they can't reproduce. They are not the same species, however, and some--not all--interspecies hybrids have infertile offspring^.) It seems that other traits are also important for defining species: such as structure and lifestyle, but it's a work in progress (and they move things around taxonomically sometimes).
^It should be noted that you can have diploids and tetraploids (or greater) of the same species of plant (thanks, in part, to chromosome doubling chemicals), and their offspring aren't fertile (but if you doubled the chromosomes of the offspring, they would be).
None of the higher ranks guarantee sexual compatibility (even if it sometimes can happen). However, chromosome doubling and such aside, you can generally expect members of a species to be compatible with confidence.
In summary, it sounds like members of the same species tend to reproduce with each other over another species when given the chance (but there's no guarantee they can't and won't breed with other species, generally speaking; you can evaluate that on a case-by-case basis, however). Each species tends to have a certain set of traits (and habits) that set it apart. But, we're still figuring everything out.
That's what I gather, anyway.


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Effects of mushrooms on their hosts
I learned that mushrooms are normally classified as either decomposers or symbiotes. I would like to know the differences between the two types and whether they are detrimental or beneficial to their host, often a tree.

where have you looked for answers so far?

I have read an article (https://sciencing.com/role-fungi-play-food-chains-13253.html) and their separate wikis.

They are saprophytes/ saprotrophs / parasitic / symbiont. Of type.

It probably makes sense to classify mushrooms (fungi) in two separate ways:

symbiotic vs. free-living: symbiotic organisms are those that live in close association with a host (etymologically sym="with", biosis="life"), free-living organisms don't.  So a mycorrhizal fungus that lives within or on the surface of a plant root is a symbiote; a fungus that lives in the soil is free-living.
mutualistic (benefiting from and benefiting a host) vs. parasitic (benefiting from but harming a host) vs. saprotrophic (consuming already-dead material; these are your "decomposers"). (Commensalism [benefiting from, but neither hurting nor harming, a host] is  a fourth possibility.) Mycorrhizal fungi are generally mutualistic. Fungi like chestnut blight or the genus of phythophthora, which includes the organism that causes potato blight, are pathogens; so are the myco-heterotrophs. Fungi such as wood-decay fungi are saprophytic.

To answer your question, species of fungi that are associated with trees may be either mutualistic (e.g. mycorrhizal fungi) or parasitic (e.g. chestnut blight).

Parasitic fungi might also be called pathogenic (i.e., disease-causing)
In popular speech, "symbiotic" is synonymous with "mutualistic" (i.e., organisms that benefit each other); in biology, however, it may refer to either a parasitic or a mutualistic organism. An individual symbiotic organism is often called a "symbiont".
In general, saprotrophs would be free-living (since they don't get their resources from a host, it doesn't really make sense for them to live on a host)
Individuals of a some fungal species can switch lifestyles/categories depending on their environment: these are called facultatively mutualistic/commensal/parasitic, e.g. see Redman et al. 2001.

Redman, Regina S., David D. Dunigan, and Rusty J. Rodriguez. “Fungal Symbiosis from Mutualism to Parasitism: Who Controls the Outcome, Host or Invader?” New Phytologist 151, no. 3 (2001): 705–16. https://doi.org/10.1046/j.0028-646x.2001.00210.x.