This blog has been dead for quite some time- life gets weird and busy, and unfortunately that means time is spent elsewhere. I am considered āessentialā in the current situation, so that means I havenāt had the time of lockdown to start back up.
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 (Iām 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.
Thatās it, thatās all Iāve got. The ask box is staying closed, because I donāt 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.
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The interior of a Eukaryotic Cell, from the outer membrane through the cytosol to the nucleus.Ā All molecular structures are colored by their function; the cytoskeleton is blue, membranes are green, ribosomes are purple, RNA and spliceosomes are pink, DNA and nucleosomes are yellow.Ā This cell is producing antibodies, all steps of the process are visualized in order from the bottom to the top of the image.Ā
Ā Ā Ā Ā Ā First DNA is transcribed to RNA, and the RNA is spliced before leaving the nucleus through a nuclear pore.Ā Translation begins when the RNA becomes bound to a ribosome, which converts the genetic sequence to a linear protein.Ā The proteins are folded and sorted inside the Golgi Complex, and then packaged into vesicles by the geodesic Clathrin Assembly.Ā These vesicles are pulled along microtubules by kinesin motors.Ā The vesicles then fuse with the outer membrane, and the antibodies are released into the bloodstream.
Hello everyone, I am back with another information post! This one is somewhat in response to a number of questions Iāve gotten that relate to ājunk DNAā, and I wanted to clear up some misconceptions.
The concept of junk DNA is a fairly old one, and came from when scientists didnāt 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 isnāt a lot of space inside the cell for them to have any extraneous DNA floating around. If a gene isnāt 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. Letās go back to my previous info post and look at the structure of a eukaryotic gene from there:
Thereās quite a bit more here that wouldnāt be considered part of the āgeneā, 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 āthese are not coding, they produce no protein, what is the point?ā, and they were labelled ājunk DNAā. As well, a lot of these supposedly ānon-codingā 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 werenāt 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 havenāt 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 wonāt 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 doesnāt cause any harm. To lose these non-coding regions would be catastrophic, because it simply wouldnāt be possible for our DNA repair mechanisms to keep up with the number of mutations being thrown at them.
I think Iāve fairly effectively driven home this point now- there isnāt really anything that geneticists consider ājunk DNAā (the term more commonly used now is ānon-coding DNAā), and to lose these regions would have a negative impact on the organism that it affected. Itās unfortunately a myth that a lot of science education hasnāt quite caught up to correcting yet!
Thanks so much for reading, and Iāll be back in about a month with āHow to Draw and Use Punnett Squaresā!Ā
(If you would like to read more things like this, I have linked to the masterlist here.)
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 Iām not getting a lot of answers about, so Iām taking a break. Iāve been informed that the issues are most likely stress-related, so Iām 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 Iām taking a break from answering asks. They take a lot of time and research, and I just donāt really have the energy right now to stay on top of them. Currently thereās over 100 unanswered questions that I would love to get to, but I also want to dedicate my full effort to them and thatās 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!Ā
Thanks to everyone (over 3000 of you!!) for your patience and understanding. Iām really hoping that this will pass quickly and I will be back to my old self sooner rather than later.
Hello! I was wondering if you'd help me with my dragon species. In my story I have many breeds of dragons of many colors, powers, etc that makes up each species. I have it that when two dragons crossbreed the offspring typically take after one breed (with few traits of the other breed) rather than them being a hybrid/mutt of the two species. And to get a true hybrid of the two breeds it may take several generations of crossbreeding. Is this realistic at all? If not, what would be? Thank you!
Hey there! Sorry, I have a bit of confusion about this question- if these are hybrids of two species thatās one thing, that Iāve somewhat addressed over here, but if these are two different breeds thatās a whole other. Because I talked about hybrids of different species earlier, Iāll address the breed thing here.
As far as getting a ātrue hybridā, there isnāt really a concept of this, at least in genetics. As soon as you cross two species or breeds, thatās a hybrid.
As far as only some traits coming through in your cross, thatās definitely possible! There would be some dominant traits/alleles inherited from each of the parents, and those would show up in the offspring, and itās possible for one parent to pass on more dominant traits than the other. So I think that overall this is a fairly realistic scenario (barring the whole ādragonā thing of course :D)
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Is it possible for a virus or bacteria to affect genetic changes in the people it infects?
Hello! Yes, it is completely possible, and fairly well documented as well, and Iāve 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 cellās enzymes to replicate. Once in the cell, some viruses can integrate themselves into that cellās 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.
I have read that real life hybrids usually had birth defects or medical problems. What kind of complications could they possibly have?
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 āhybrid vigourā or āheterosisā. 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).
I hope this helps to answer your question, even though itās basically the opposite of what you asked. I think you might have been thinking of a specific example that I am more than happy to look into if you provide it!
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 Iām 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
Ā Mutations cause changes to our genetics and ultimately create all of the beautiful and fascinating variation we see in the living world around us, and even within ourselves as a species. Iām going to talk about the three kinds of point mutations today, and touch on the larger scale mutations that occur.
Quite often when people think of mutations, they are only really thinking of point mutations. One small change, and BAM! you have a whole new phenotype. This is rarely the case, but the accumulation of point mutations over time can cause a ripple of change. Thereās three main types:
Silent- the most boring. Basically one base pair is changed out for another, but the resulting codon is changed, so, essentially, there is no change to the genetic code
Missense- a little more exciting. One base pair is changed for another, and causes a different codon. I spoke about Sickle-cell anemia in my last post, and this is an example of a missense mutation.
Nonsense- a base pair is changed out, but this time results in a stop codon. This can be quite catastrophic if it happens early in the coding region, because the resulting RNA and protein will be much less than what they should be.
Thatās the point mutations for you! Because I wanted to avoid getting this too long, I wonāt be giving examples, but a quick Google search could provide you plenty in humans and other critters.
The larger scale mutations fall into three basic categories: too much DNA, too little DNA, and DNA a little to the left. Iāll explain what all of this means!
Too much DNA- there are two possibilities here. Either there was an insertion of some DNA from a different part of the genome, or when the DNA replicated there was an accidental duplication, repeating the part that just came before it. These vary wildly in their results, either having no effect whatsoever, or interrupting the coding region and not allowing the DNA to be read properly there.
Too little DNA-Ā mass deletions are also possible. For example, sometimes when DNA is being replicated, the proteins doing the replication āfall offā and it is not completed properly. We have a lot of failsafes in place to catch these errors, but sometimes they do slide through. Again, the results can be very bad or very neutral, depending on what genes were in that region.
DNA a little to the left- this is probably the most confusing, but if the reading of the coding region starts one or two base pairs over from where it should, we get a āframeshift mutationā. This usually results from the deletion or insertion of one or two basepairs, and I found a really great image to help out my explanation:
Codons are always read in groups of three, so either inserting or deleting one nucleobase out of the coding/reading area results in complete nonsense!
So, thatās pretty much it for mutations. A lot of this is going to come up again much later when I talk about genetic editing, because we use a lot of these principles for our own devices when creating genetically modified organisms.
Thank you so much for reading, ask away on the questions, and you will see one of these info posts again later this month with āThe Myth of Junk DNAā
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 Iām 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 Iām 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 āGeneā 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: Itās Time We Talk About Alleles
I think probably the most common question I get, both here and professionally is phrased something like this:
āSo I want my population of X to have blue-eyed genes, and most the population has brown eyes, how does that work?ā
To be clear, there is absolutely nothing wrong with this question. Itās completely legitimate, and itās my job as a science educator to develop all of my readersā understanding of how genetics works.
But first. We need to talk about how proteins are coded. Itās something I specifically avoided in the last post because it was getting too long!
I spoke a bit about how DNA is transcribed into RNA. That part is very neatly and āeasyā. The DNA is opened up, and proteins move along the DNA stranding, building a short RNA strand that represents the coding region of DNA. The only major difference that matters for our understanding is that in RNA Uracil is used in place of Thymine. A U instead of a T!
Then we move to Translation. And the big question is how do we move from RNA to protein? And the answer is relatively easy to lay out: every set of three nucleobases represents one animo acid to the ribosome! These are called codons.
What. Okay. Letās get a chart:
So in this chart, the upper case letters (which if you look close are all either A, C, G or U), are the RNA nucleobases. The lower case letters are shorthand for each amino acid (I couldnāt find a good chart that had the whole name of each animo acid written out, my apologies for that). Three of these codons (UAA, UAG, UGA) say āstopā instead. This is a stop codon, and represents the end of the amino acid chain being produced. AUG is our āstartā codon, and represents where the protein actually starts. When transcription occurs, thereās usually a bit of extra that is transcribed at the beginning, so this tells the ribosome where the protein actually begins.
So what does this have to do with alleles? Alleles are variations within the same gene. For simplicityās sake, Iām going to use an example that involves only a single nucleobase change, or point mutation:
Sickle-cell anemia is a fairly well-known example of this. At the sixth codon, there is a change from GAG (which makes glutamic acid as its amino acid) to GUG (which makes valine as its amino acid). This causes the whole structure of the protein produced to be different, and for red blood cells in an affected person to be U-shaped instead of the usual round disk.
Now, this is a fairly extreme example, but you can imagine how these small changes can build up over time, and create a lot of the variation and alleles we see within a population. As the changes accumulate, eventually we hit a point where a protein is changed and we see a physical difference (a whole new phenotype!). So we donāt actually need blue-eyed and brown-eyed and green-eyed genes to be all separate. Instead we can have changes on the genes that already exist and create a whole world of variation!
Thanks so much for reading! My final topic tomorrow is on mutations, how they occur and the different kinds we can have!
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 Iām 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 Iām 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 āGeneā 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
Okay, letās get the rest of that picture:
Ho man, thatās a lot more to unravel. Ā But this is essentially how genes work.
1. We start off with our DNA, and our single gene here. We have a promotor region, so the proteins that read DNA bind and read through the coding region, stopping at our terminator. When they āreadā, they are producing mRNA! So basically transcribing what is written in the DNA and producing one small molecule that can venture off and be turned into something useful. This process is called Transcription. DNA and RNA are both made of nucleobases, so this is more like writing down a passage of a book that you like in your own notebook rather than creating something new.
2. Splicing occurs. Sometimes, not every part of the coding region is used for the same thing, so the mRNA is rearranged so that all of the parts that need to used together are next to each other.
3. Ribosomes (something Iāll talk about when I talk about A Little Bit of Cell Biology) pick up this mRNA and use amino acids to build proteins. This is call Translation because, while RNA still uses nucleobases (the same language as DNA), proteins use amino acids, which are completely different. So this is translating what was originally DNA into a different language- and a product that can be used to build you and me and every living thing around us!
Three easy steps from DNA to functional organism, and the what is referred to as the Central Dogma of Genetics:
DNA - (transcription) - RNA- (translation) - protein
A couple of things to note. This isnāt as simple as sometimes genetics is made out to be on television or in the media. Thereās a lot of important steps that must be executed perfectly in order for this gene to be expressed. As well, the expression of this gene depends on several things. For example, a silencer in front would mean there is no gene expression. Or if the mRNA is not picked up by ribosomes. Or if the necessary amino acids to build the protein arenāt present at that time. Having multiple steps like this, rather then simply having every single gene be expressed means there can be a lot of very subtle cellular control over what the body is doing. Very useful!
Also, when you are looking at that second āsplicing stageā (itās the part in grey labelled āpost transcription modificationā), notice that there are two little grey pieces in the middle of the red both labelled āintronsā. Those are pieces that can either be coding or non-coding depending on the situation. Sometimes they will buddy up and be translated into protein, sometimes they are just junk that is tossed aside and broken down. Introns can do many things for us, but one important function is they can act as a buffer against mutations, by essentially making sure that if a mutation does occur in that region it has less of a chance of hitting a more important coding region. Having gaps where there is no coding actively occurring is so important for the health of the DNA. Lots of places without coding can be the difference between every mutagen interrupting a process and 99% of mutagens hitting nothing but non-coding pieces.
Thanks for reading this. Tomorrow we are going to talk about āallelesā, what that means and why we can have variation without needing to introduce new genes.
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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 Iām 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 Iām 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 āGeneā 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, letās dive in.
Part I: When I say āgeneā and you say āgeneā sometimes we mean different things
I talk a lot about genetics. I talk about it with my family, my friends, on the internet, and at work. Itās my absolute favourite thing to discuss with basically anyone, and what Iāve learned the most from these discussions is that when I say the word āgeneā and when people who donāt have a genetics degree say the word āgeneā, sometimes we are talking about two different concepts. This is in no way the fault of the people who donāt have that degree, but I do think it leads to some pretty major breakdowns in communication. A scientist says one thing, and the media report on it means another, further perpetuating the misinformation. Which is why I think this is such an important post to make!
What Iāve found is that when most people talk about genes, they would define a gene as āsomething in your DNA that encodes for a trait.ā Which isnāt precisely correct, but back when we were first discovering that genes existed, was the basic working definition. However, if you were to ask me what a gene is, I would probably reply āa functional unit of DNA or RNAā. Which is really not helpful to anyone, but the actual answer is going to take all of these posts!
What I mean when I say a āfunctional unitā is something that, within your DNA, contains everything required to code for something that has a function. This would include three main parts: a promotor, an encoding region, and a stop sequence. This doesnāt necessarily have to cause a trait directly- perhaps it encodes for a protein that acts as a silencer on another gene, or in fact, encodes for two different proteins at the same time, one that produces a protein that directly influences hair colour, and another that enhances another gene by acting directly on its promotor.
Okay, letās get a picture of what Iām talking about:
This is what I picture when I picture a gene. Actually basically exactly this image, because itās from wikimedia commons, so pretty much every professor I ever had used it in their lectures. So, most of the time when people talk about āgenesā they are referring to that āprotein coding regionā, which, as you can see, is only really half the story.
Thereās the promotor, one example of which is the āTATA-boxā I talked about in my previous post. This is the āgoā region. Essentially it acts as a place for other proteins to bind that open and read the coding region. Generally this is referred to as a non-coding region, because it doesnāt actually code for something in particular (that is reserved for protein coding regions), but it is still very essential, because it marks the spot where a coding region starts. At the end as well, you see that little blue bit that makes up the āterminatorā (sorry that part got cut off). That marks the end of the coding region. Without that, the proteins that are reading this DNA would just keep going and going into what they were reading devolved into nonsense.
As well, note the section labelled āupstream operatorā before any part of this even starts. When we discuss gene regulation, I will get more into how those work and why they are important, however, they are not generally considered part of the gene itself.
This is sometimes where there is some confusion- quite often people picture mutations in genes or changes to the genome in genetic modification as simply editing what the DNA says, but in reality itās much more complicated (and also much easier!) than that. For example, if I want to āturn a gene offā, I donāt necessarily need to cut it out completely, but instead can interrupt the promotor, or use an upstream silencer that doesnāt allow my gene of choice to be read. Alternatively, I can interrupt the terminator so that everything read out of that coding region is completely nonsense and useless to the cell (or catastrophic depending on what I do). Alternatively, I could insert an enhancer region either upstream or downstream of my coding region and have my gene of choice be expressed at a much higher level than before.
Okay, so thatās the very first part of this story, and covers the basics of how a gene is structured. Tomorrow we are going to delve into how this gene turns from a DNA sequence into something that can actually be used.
Hey everyone!
Iāve been out for about a week, and my apologies for that. I had a couple of small but very time-consuming family emergencies come up (everyone is fine though, no worries there!), combined with some truly horrendous weather that doubled (or tripled) my commute time, meant Iāve had about 0 time to update this blog.Ā
On the bright side, Iām baaaack! Iām working on some answers to the asks that keep piling up (and keep sending them in!), as well as myĀ āWhat is a Geneā post, that has turned into a bit of a monster.
On that note, what Iām going to do for that post is split it into four parts, and post those parts separately, because I think itās a bit overwhelming to take it all in at once. So youāll see one part per day for the rest of this week, and Iāll be sure to link them back in the original Information Post... post.
Thanks for your patience, I promise Iām still here. Just a little less here than usual.
Would genetic engineering leave marks on the genome? I have people who are genetically engineered to express a trait codominantly, so will this show up when they get genetically tested?
So, this sort of depends what you mean by āmarksā. There isnāt 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 isnāt 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!
in korea itās actually very important whoās born earlier! bc you have to call them either oppa (female to older male), hyung (male to older male), unni (female to older female), or noona (male to older female). i always forget that some other cultures donāt do this, also i think it would just be weird to ask whoās older if it werenāt needed. usually ppl in korea can figure out whoās older by listening to who calls the other one of the names above, although some twins donāt do it
Since at least the last common ancestor of all life on Earth, genetic information has been stored in a four-letter alphabet that is propagated and retrieved by the formation of two base pairs. The central goal of synthetic biology is to create new life forms and functions, and the most general route to this goal is the creation of semi-synthetic organisms whose DNA harbours two additional letters that form a third, unnatural base pair. Previous efforts to generate such semi-synthetic organisms culminated in the creation of a strain of Escherichia coli that, by virtue of a nucleoside triphosphate transporter from Phaeodactylum tricornutum, imports the requisite unnatural triphosphates from its medium and then uses them to replicate a plasmid containing the unnatural base pair dNaM-dTPT3. Although the semi-synthetic organism stores increased information when compared to natural organisms, retrieval of the information requires in vivo transcription of the unnatural base pair into mRNA and tRNA, aminoacylation of the tRNA with a non-canonical amino acid, and efficient participation of the unnatural base pair in decoding at the ribosome. Here we report the in vivo transcription of DNA containing dNaM and dTPT3 into mRNAs with two different unnatural codons and tRNAs with cognate unnatural anticodons, and their efficient decoding at the ribosome to direct the site-specific incorporation of natural or non-canonical amino acids into superfolder green fluorescent protein. The results demonstrate that interactions other than hydrogen bonding can contribute to every step of information storage and retrieval. The resulting semi-synthetic organism both encodes and retrieves increased information and should serve as a platform for the creation of new life forms and functions.
A very nice paper, and a late contender for my Favorite Paper of the Year.
On an unrelated note, sci-hub is currently living atĀ https://sci-hub.bz/Ā ā¦.
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I am a big fan of plausible "scientific" explanations for myths and supernatural shenanigans. So ... werewolves. Suppose the genome for a wolf were somehow encoded in the so-called "junk DNA" and there was some mechanism by which the wolf DNA starts being expressed and the human repressed. What would happen if suddenly every cell in my body had wolf DNA? ...I expect an ugly death, but if so, what might be the first few steps before death?
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 āwolfā the new blood cells produced would all be for wolves. This wouldnāt be an issue for the new cells, because the immune system would label them as āfriendā rather than āinvaderā, but for all of the red blood cells still in the body this would be bad news. Red blood cells donāt have nuclei, and therefore donāt 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.
Thanks for this question, and if anyone else has any theories, toss them in the reblogs and replies! This was my best guess, I would love to see what other people think!
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 Iām 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 āwhat is a geneā, 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 donāt 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. Letās 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- itās elegant in both design and function.)
This can be broken down into two main parts:
The phosphate-sugar backbone (all those Pās and Oās 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 youāve heard DNA being described as ācomplementaryā, 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 āreadā 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, thereās 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!). Itās not a terribly complicated design, which is probably why it is so immensely biologically successful.
So, there we have it: a very, very quick rundown that is mostly to get some important features pointed out before I talk about what a gene is, and how DNA encodes them on January 31st. This is hardly comprehensive, but I will get more in-depth into the structure and features then, and I didnāt want to make that info post horrendously long. Thanks for reading!
