Species Counseling

That being said, a lot goes on in the world even while many of us feel like we should be sitting still.

I am not a person of colour, so, to be clear, this statement will not be about how I think we should be supporting others in their movements, or what we as a collective should be doing (I’m also not American, and that limits my immediate knowledge of what should be done). I strongly encourage you to reach out to your local BLM chapters or donate to those who are fighting injustice either in your location or on a national level. At the end of the day, racism is a detriment to us all.

What I will say is on the topic of genetics.

Your genes do not define you. Others genes do not define them. At the end of the day we are all moving masses of cells and electrical currents, and no one, and I do mean no one, is lesser because of their genetics. There has never been a valid study to show this, and there never will be, because while scientists can be awful, and subject to all of the prejudices that are tragically present in our society, the science still speaks truth. If you are looking at something, and it seems to be slanted against any group of people, ask questions. What was the study trying to prove? Who benefited from it? Who funded it?

We can all get better. We can all do better. And we can all do this together. Stand up for yourself. Stand up for your neighbour. Make space for the voices that have been suppressed, and most importantly, learn from this experience.

That’s it, that’s all I’ve got. The ask box is staying closed, because I don’t have time to answer questions coming in with the honesty and integrity they deserve. However, this is a fairly large platform, and I believe silence sits next to complacency.

Hello everyone, I am back with another information post! This one is somewhat in response to a number of questions I’ve gotten that relate to “junk DNA”, and I wanted to clear up some misconceptions.

The concept of junk DNA is a fairly old one, and came from when scientists didn’t have a great understanding of how genes worked. When genetics got its start as a science, we looked primarily at bacterial genomes, because they are small, easy to get, and we can have lots and lots of identical organisms. And when we looked at bacterial genomes they looked something like this:

Lots of bacterial genomes are circular, like our friend A. arilaitensis here. And each of those colourful rectangles around the edge represent a coding region for a protein. Bacteria have extremely dense genomes with regards to the amount of protein coding regions and proteins that they produce, but they have to be. There just simply isn’t a lot of space inside the cell for them to have any extraneous DNA floating around. If a gene isn’t being used, then it is removed, which is in sharp contrast to higher organisms that can keep genes around just for the fun of it (and in case it becomes useful later, or if the environment changes).

So with bacterial genomes in mind, we can shift our attention over to some very different genomes. Let’s go back to my previous info post and look at the structure of a eukaryotic gene from there:

There’s quite a bit more here that wouldn’t be considered part of the “gene”, but are still important- the upstream and downstream enhancers/silencers, as well as the introns are not coding regions but are equally important to expression. However, when we first studying these genes, the people looking at it went “these are not coding, they produce no protein, what is the point?”, and they were labelled “junk DNA”. As well, a lot of these supposedly “non-coding” regions were found later to have other important functions related to DNA storage within the cell, as well as epigenetics.

To further this, not every non coding region has a function either. We do also have long stretches of basically nothing that still serves an important function in protecting us from harm.

The first and foremost of these are the telomeres, found on the ends of each chromosome. Because of how DNA replicates in our cells, a little bit is lost off of the end each time, just the space that it takes for protein to bind to begin replication. If it weren’t for these telomeres, we would very rapidly start losing coding regions of DNA, and interrupt some very important cellular processes.

The other areas that are more central in the chromosome mainly function as a buffer region in case of mutation (or we haven’t found the function yet!). There is a certain level of mutation expected with every replication (it varies from organism to organism, some are better at replication than others), as well as from environmental factors (UV rays, other types of radiation, stress on the organism, etc), so by having lots of areas where there are no genes being coded, it increases the chances that mutations will happen where it won’t make a difference to the function of the organism. Bacteria frequently pick up catastrophic mutations during binary fission, but because they replicate so quickly that organism will be quickly replaced (listen, the bacterial lifestyle is a harsh one). In more complex organisms, a lot more energy is invested into ensuring that DNA is replicated correctly, or at least in a way that doesn’t cause any harm. To lose these non-coding regions would be catastrophic, because it simply wouldn’t be possible for our DNA repair mechanisms to keep up with the number of mutations being thrown at them.

I think I’ve fairly effectively driven home this point now- there isn’t really anything that geneticists consider “junk DNA” (the term more commonly used now is “non-coding DNA”), and to lose these regions would have a negative impact on the organism that it affected. It’s unfortunately a myth that a lot of science education hasn’t quite caught up to correcting yet!

Thanks so much for reading, and I’ll be back in about a month with “How to Draw and Use Punnett Squares”! 

Hey everyone! If you try to submit an ask right now, you will notice that the ask box is closed. I ran into some highly unexpected health problems last week that I’m not getting a lot of answers about, so I’m taking a break. I’ve been informed that the issues are most likely stress-related, so I’m cutting back some of my extracurriculars in hopes that will help nip this issue in the bud before it turns into something more serious. What that means for this blog is that I’m taking a break from answering asks. They take a lot of time and research, and I just don’t really have the energy right now to stay on top of them. Currently there’s over 100 unanswered questions that I would love to get to, but I also want to dedicate my full effort to them and that’s just not in the cards right now.

What I am going to be doing is continuing the Info Posts! They are once monthly, and are a bit less research heavy than asks, mostly because I chose topics that I can pull information from my own education and experience. So, you will still see those!  Thanks to everyone (over 3000 of you!!) for your patience and understanding. I’m really hoping that this will pass quickly and I will be back to my old self sooner rather than later.

Hey there! Sorry, I have a bit of confusion about this question- if these are hybrids of two species that’s one thing, that I’ve somewhat addressed over here, but if these are two different breeds that’s a whole other. Because I talked about hybrids of different species earlier, I’ll address the breed thing here.

As far as getting a “true hybrid”, there isn’t really a concept of this, at least in genetics. As soon as you cross two species or breeds, that’s a hybrid.

Hello! Yes, it is completely possible, and fairly well documented as well, and I’ve got a viral example for you!

Viruses are basically freeloaders. They have very tiny genomes, and need to use the cells that they infect to reproduce for them. They do this by injecting DNA (or RNA) into the cell, and using the cell’s enzymes to replicate. Once in the cell, some viruses can integrate themselves into that cell’s genome, promote other genes or produce their own proteins. One virus that does this is Human Papillomavirus (HPV). Once in the cell, it can promote tumour growth, cell growth and prevent cell death, all of which are favourable conditions for cancer to develop.

Hi! Hybridization is a bit of a tricky topic, because there is a lot of possibility in the types of crosses you are getting. Some hybrids, like mules, are infertile because there is a difference in chromosome number between horses and mules. However, they are generally very healthy and are very successful without major health issues.

Other hybrids, such as the grizzly/polar bear crosses we are starting to see in the northern parts of Canada and in Alaska are very successful in their environments and can sexually reproduce with each other, as well as backcross to their parent species. This has lead to the start of a new species of bear that is much more suited to its changing environment.

So these are two examples where hybridization does not cause any problems, and in the latter case actually creates an animal that is actually better fit for its environment than either of the original species. This is generally the more likely result with hybridization, which we also refer to as “hybrid vigour” or “heterosis”. Basically by creating these hybrids we can quickly introduce new genes and genetic variation, and, as a general rule, variation is strength. So while it is possible that there issues, usually we see stronger organisms (at least in nature).

This is the second of thirteen more in-depth write-ups I have planned out for this year. The list (which is not set in stone!) can be found here.

I decided to do these as a way to get more information out to the readers here without having to delve into one specific ask or series of questions. I can imagine that these might create more questions as I go, but I’m also hoping that they will provide a resource that readers can refer back to. The general idea is to allow the series to build up in complexity, and give everyone a better understanding of these topics!

Okay, the final one of this series!

Part IV: Mutations

This is the second of thirteen more in-depth write-ups I have planned out for this year. The list (which is not set in stone!) can be found here.

I decided to do these as a way to get more information out to the readers here without having to delve into one specific ask or series of questions. I can imagine that these might create more questions as I go, but I’m also hoping that they will provide a resource that readers can refer back to. The general idea is to allow the series to build up in complexity, and give everyone a better understanding of these topics!

This post is going to be quite a bit longer than my last one, so I’m going to throw it under a read-more for ease of Tumblr browsing. There will be four main parts to it, and hopefully by the end, all of you will feel much more comfortable with what a gene actually is! These parts will post separately, because this whole thing turned into so much more than I was expecting when I was planning it out.

Part I: When I Say “Gene” What Am I Talking About?

Part II: The Central Dogma of Genetics (a.k.a. how a gene works)

Part III: Alleles

Part IV: Mutations

Part III: It’s Time We Talk About Alleles

This is the second of thirteen more in-depth write-ups I have planned out for this year. The list (which is not set in stone!) can be found here.

I decided to do these as a way to get more information out to the readers here without having to delve into one specific ask or series of questions. I can imagine that these might create more questions as I go, but I’m also hoping that they will provide a resource that readers can refer back to. The general idea is to allow the series to build up in complexity, and give everyone a better understanding of these topics!

This post is going to be quite a bit longer than my last one, so I’m going to throw it under a read-more for ease of Tumblr browsing. There will be four main parts to it, and hopefully by the end, all of you will feel much more comfortable with what a gene actually is! These parts will post separately, because this whole thing turned into so much more than I was expecting when I was planning it out.

Part I: When I Say “Gene” What Am I Talking About?

Part II: The Central Dogma of Genetics (a.k.a. how a gene works)

Part III: Alleles

Part IV: Mutations

Alright, onto Part II! Part II: The Central Dogma of Genetics

This is the second of thirteen more in-depth write-ups I have planned out for this year. The list (which is not set in stone!) can be found here.

I decided to do these as a way to get more information out to the readers here without having to delve into one specific ask or series of questions. I can imagine that these might create more questions as I go, but I’m also hoping that they will provide a resource that readers can refer back to. The general idea is to allow the series to build up in complexity, and give everyone a better understanding of these topics!

This post is going to be quite a bit longer than my last one, so I’m going to throw it under a read-more for ease of Tumblr browsing. There will be four main parts to it, and hopefully by the end, all of you will feel much more comfortable with what a gene actually is! These parts will post separately, because this whole thing turned into so much more than I was expecting when I was planning it out.

Part I: When I Say “Gene” What Am I Talking About?

Part II: The Central Dogma of Genetics (a.k.a. how a gene works)

Part III: Alleles

Part IV: Mutations

Without further ado, let’s dive in.

Part I: When I say “gene” and you say “gene” sometimes we mean different things

So, this sort of depends what you mean by “marks”. There isn’t going to be any specific indicator that the genome was changed, however, the inserted/removed/changed gene will now show up if sequenced. Basically what that means is if I sequence my organism before doing any gene editing, and then sequence it after inserting my new gene of choice, I will see that inserted gene. But we are inserting the same type of material (nucleobases!) that DNA uses, and quite often use the same enzymes and proteins that are normally present to help the process along. So there isn’t going to be some sort of break or interruption preceding or following my inserted gene- it will look as though it belonged there the whole time!

This is quite an interesting question (not in a bad way at all!), and I had to think about it for a bit. I think you are on the right track with the ugly death, but not necessarily for the reasons you might think, and this was honestly mostly me searching a whole bunch of things that I thought would be different between humans and wolves to try and figure out what would kill you first.

I think the most likely cause of death would be a blood type incompatibility. Canines have completely different blood types than humans, and if the all the cells suddenly switched over to “wolf” the new blood cells produced would all be for wolves. This wouldn’t be an issue for the new cells, because the immune system would label them as “friend” rather than “invader”, but for all of the red blood cells still in the body this would be bad news. Red blood cells don’t have nuclei, and therefore don’t have DNA in most mammals, so they would still be expressing human antigens of whatever blood type the person is (A, B, AB, or O), and would be attacked by the new immune cells. Blood type incompatibility is not nice: expect heavy clotting as red blood cells are broken down, stroke and renal failure.

This is the first of thirteen more in-depth write-ups I have planned out for this year. The list (which is not set in stone!) can be found here.

I decided to do these as a way to get more information out to the readers here without having to delve into one specific ask or series of questions. I can imagine that these might create more questions as I go, but I’m also hoping that they will provide a resource that readers can refer back to. The general idea is to allow the series to build up in complexity, and give everyone a better understanding of these topics!

What is DNA?

This first topic is going to be relatively short, because in a couple of weeks I am going to do “what is a gene”, which will get much longer and more complicated, but I wanted some set up about the physical structure of DNA.

You might have heard DNA described in a lot of different ways. Deoxyribonucleic acid. The building blocks of life. The blueprint of You. None of these are particularity inaccurate, but I don’t think that any of them are super great descriptors of what exactly DNA is, or how exactly it goes from existing in cells to encoding entire organisms (although I am going to talk about the actual encoding part in the future).

For now, we are going to start small. Let’s only look at the actual physical structure. Here we have a DNA molecule:

image from wikimedia commons here

So beautiful! (I might be biased, but DNA is my favourite molecule- it’s elegant in both design and function.)

This can be broken down into two main parts:

The phosphate-sugar backbone (all those P’s and O’s and light blue on the outside)

The nucleobases (adenine [A], thymine [T], cytosine [C], and guanine [G]- the purple, pink, yellow and green)

I will point out the hydrogen bonds in the middle as well. Note that cytosine and guanine have three bonds between them, and adenine and thymine only have two. These molecules always bond in this pattern (A bonds to T, and C to G). If you’ve heard DNA being described as “complementary”, this is why! If you find a C on one strand, you know that you will find a G on the other (this became very important for sequencing, but we will talk about that later).

The hydrogen bonds in the middle are quite important as well. If these molecules were bonded to each other directly, it would be basically impossible to open the strand to “read” the DNA. Instead, this can be done by breaking those hydrogen bonds, and then allowing them to reform. This does mean that a mutation is much more likely in a high A-T region rather than a high C-G on, simply because A-T only has two bonds, and C-G has three. As well, quite often before a gene is encoded, there’s a long stretch of TATA- repeated (these are cleverly called TATA-boxes), so that the strand can more easily be opened and the encoded gene read. More on that when I talk about what a gene is!

And that is honestly pretty much it for DNA (I say that in jest- there is a lot more, and this is the result of a few billion years of evolution!). It’s not a terribly complicated design, which is probably why it is so immensely biologically successful.