(biologist - artist - queer)

  • tea
  • anime
  • tabletop

You’re the only magician that could make a falling horse turn into thirteen gerbils

  • 1 Post
  • 28 Comments
Joined 1 year ago
cake
Cake day: June 10th, 2023

help-circle




  • When I say “the cell isn’t a machine”, it is in specific reference to the machine model of the cell, which is a previously established conceptual framework in the field of molecular biology. If you want to understand why that model is falling out of favor today, you’re invited to read the article linked by OP and/or the articles I have linked in other comments.

    The gist is that the cell is more complicated, flexible, and emergent than any machine has ever been and will be for the foreseeable future, and the idea that we can simply map the functions of each molecule in the cell to get a perfect “circuit diagram” of how everything plays together is defunct.

    I don’t have time to mess with this thread any more. You can either accept what myself (an expert in this field), the author of this publication (which happens to be one of the most prestigious journals in the world), and others who do this research daily are saying about this, or you can not. Frankly, if you are an expert also, the field, the research, and the truth barely cares about our opinion-- it certainly doesn’t care about non-expert opinions on the internet.


  • Junk DNA is repeating codons, or codons that occur in areas that are outside of the “start/stop” codon triplicate pairs.

    Those sequences do things and have effects. In fact, the coding regions are often less functional than the non-coding ones.

    They aren’t there for structural reasons, all DNA is the same 4 codons linked together over and over, all the different chromosomes are different sizes.

    Sometimes they ARE there for structural reasons? Read: enhancers, or CTCF binding sites? Among many other myriad examples of functional noncoding regions? Also, nucleotides =/= codons. There are 64 codons.

    All of this DNA is reported when the cells divide, that’s the only time those regions between the stops and starts actually come into play. This is very easily proven, we know the structure of the reading proteins down to the molecule (indeed there are starts and stops and triplicate base pairs that design these transcribing proteins).

    That’s bull. You’re out of your depth. A contemporary college molecular biology course would show your examples to the contrary.

    The “important” junk DNA that has significance while not being in a “start->stop” zone are the codons that occur before the first start codon on either side of a DNA strand, when DNA is replicated the protein that starts replicating it has to start at 1 end of 1 side of the DNA in order to be able to read it

    I feel like a broken record but Enhancers! lncRNAs! siRNAs! Binding sites! Other gene regulatory regions! Epigenetic nucleosome modifications! Chromatin remodeler sites!

    except it needs to find the end first, and to make sure it’s all the end it “clips” the first 6 (? Maybe more maybe less, it’s been decades since I’ve studied this)

    Oh, there’s your problem. A lot has changed. You refuse to see the sea change happening around you because it means you’re out of date.

    Sorry for the wall of text, but there’s plenty of examples of blatantly junk DNA, and there are known methods of how it occurs. Anyone who says every codon pair has a purpose has a screw loose and is ignorant to the mechanics of evolution.

    I was happy to reply to you and engage pleasantly originally but you are only engaging with people that know less about biology than you do. You are not an expert if you last studied biology decades ago and can’t remember the details. You certainly aren’t enough of an authority on the subject to question a contemporary article published in Science or the work of other researchers currently in the field.

    I really, really encourage you to read these papers thoroughly. You are the target audience-- people who learned the machine model of the cell and who are gripping it so tightly that they are blind to the nuance that we’ve uncovered. I also encourage you to not write insults about people who disagree with you, especially people with more domain knowledge than you have.


  • This is a funny comment though, because “junk” DNA is involved with epigenetic regulation and cellular behavior.

    “It’s there so it must have function”, “it’s still in the genetic code so it must have been selected for” is the least nuanced take,

    “It’s there just randomly and therefore is junk”, and “evolution does not select for efficiency” is an improvement,

    But “it’s there and it’s doing something despite not having a bespoke, prescribed function” and “evolution is a cascade of emergent effects and random chance, none of our genome is non-functional even though it is random” is the most up to date take

    You seem like a biologist, why not go read some of these papers? Like the one I linked by Dan Nichols? Most people don’t have the background necessary to understand the language (no shade) but you seem to!


  • I would encourage you to read the linked Science paper and Dan Nichol’s paper, Is the Cell Really a Machine?

    You feel that if a codon isn’t meant for something, if it doesn’t have a purpose– then it is junk. This is a mindset that is reflective of the machine model of the cell. We used to expect that each protein was bespoke for a function, each transcript necessary.

    The whole paradigm shift at hand is this model falls flat, even for coding regions. I think you’re actually very spot in here with the prokaryotic DNA or the plant genomes (love me some violets for their weird genomes). Some parts of a genome will rapidly change and appear to serve no real purpose, but the next bite is the important one: even if it seems like there isn’t a purpose, like a top-down prescription for functionality, those regions are still doing something while they are present.

    For example, some long non-coding regions affect the likelihood that a person will develop Parkinson’s disease, or in the case of plants with various polyploidies, the relative expression of their genes won’t necessarily change, but the absolute expression may.

    Basically, you aren’t wrong that these regions dont have a purpose, because no genes have a purpose. The cell isn’t a machine.



  • So I think I can make the claim that I am an expert in this, at least compared to 95%+ of biological researchers. My research foci include epigenetic and emergent interactions like the ones discussed in the article, and although I am not going to back this up by identifying myself, please believe me when I say I’ve written some papers on the topic.

    The concept of junk DNA is perhaps the problem here. Obviously there are large swaths of our genome that do not encode anything or have instructions for proteins. However, dismissing all non-coding DNA as “junk” is a critical error.

    Your telomeres are a great example. They don’t contain vital information so much as they serve a specific function-- providing a buffer region to be consumed during replication in place of DNA that does contain vital information. Your cells would work less well without telomeres, so calling them junk is inaccurate.

    Other examples of important non-coding regions are enhancer and promoter regions. Papers describing the philosophical developments of stochasticity in cellular function note how enhancers are vital for increasing the likelihood of transcription by making it more likely that specific proteins floating in the cellular matrix interact with each other. Promoter regions are something most biologists understand already, so I won’t describe them here (apologies for anyone who needs to go read about them elsewhere!). Some regions also inform the 3D structure of the genome, creating topological associated domains (TADs) that bring regions of interest closer together.

    Even the sequences with less obvious non-coding functions often have some emergent effect on cellular function. Transcription occurs in nonsense regions despite no mRNA being created; instead, tiny, transient non-coding RNAs (ncRNAs) are produced. Because RNA can have functional and catalytic properties like proteins, these small RNAs “do jobs” while they exist. The kinds of things they do before being degraded are less defined than the mechanistic models of proteins, but as we understand more stochastic models, we are beginning to understand how they work.

    One last type of DNA that we used to consider junk: binding sites for transcription factors, nucleosome remodelers, and other DNA binding proteins. Proteins are getting stuck to DNA all the time, and then doing things while they’re stuck there. Sometimes even just being a place where a nucleosome with a epigenetic flag can camp out and direct other cellular processes is enough to invalidate calling that region “junk”.

    Anyway I’m done giving my spiel but the take home message here is that all DNA causes stochastic effects and almost all of it (likely all and we haven’t figured it out yet) serves some function in-context. Calling all DNA that doesn’t encode for a protein “junk” is outdated-- if anything, the protein encoding regions are the boring parts.


  • Girl, this community is full of trans folks, and not all of us are trans women. I’d wager the majority of people annoyed with this post are not cis, and it seems like some of them are trans women, too

    It’s not even something I would post in a community just for trans women, like what about trans women that don’t end up with these characteristics? Are people only trans women if they identify with these changes? Why is the assumption that men (and I guess pre-transition trans women) have anger issues and porn addictions? Why are those qualities tied to their hormones and physical bodies, so trans women who can’t or won’t medically transition are excluded from benefitting?


  • First, I want to fully admit I didn’t watch the video. Apologies ahead of time if that causes me to be redundant or reductive.

    Second, I’m also a biologist, although a molecular one.

    Third, I agree with almost all of your premise and train of thought. We’re certainly more likely to get the likes of “bacterial mats” than intelligent life anywhere, and especially within a distance that we will ever realistically encounter.

    I do wonder, though, how you (or maybe the video guy, but obviously not enough to watch the source material before making an ass of myself…) conceptually reconcile the small sample number of known planets with life (n=1) with the mindblowingly impossible number of worlds.

    You say that intelligent life evolving only once indicates that it is difficult for evolution to “discover”, which is surely possible to be true. But given that we haven’t seen the evolutionary conditions on other hypothetical worlds, from what we know, the evolution of intelligent life has a perfect 100% success rate of occurring on planets with life.

    In fact, you mention the independent convergent evolution of eyes as an indication that eyes are a “good idea”, and that they must be relatively easy for evolution to discover if they evolve independently, repeatedly. But evolution is subject to the whims of selective forces, so a different world would surely select for different traits. Eyes (or other extremely common evolutionary pathways… looking at you, crab body) might be less frequently selected for or be entirely useless, but intellegent decision making and tool use might evolve in ways we can’t even conceptualize in our context.

    This also extends to the claim of how our world is evolutionarily dynamic (which you point out is hard to quantify in context). We don’t know the dynamics of evolution on other worlds, if it happens at all. Recombination could be a unique characteristic of DNA-based life on Earth or it could be extremely common. Other worlds might have longer or shorter evolutionary time lines, also, since our sun’s “working life” is shorter than average due to its size and density. Without another example for reference, we don’t know whether we’re evolving quickly and with diversity or slowly and conservatively.

    I guess, I don’t think you are wrong, exactly. I just think you are necessarily making assumptions based on how things work here in order to extrapolate how things might work there– one has to! But the whole discussion (which continues, like this, to this day) revolves around just too many unknowns. We just don’t know, and can’t know.

    Climbing down from my high-horse, though, I have to admit I’m biased, since I have a pet-belief that life is basically guaranteed to exist elsewhere (how freakish would it be for it to only happen once out of so, so many chances?). I honestly feel like there’s a good shot that it’s incredibly common, at least in a basic form. In essence, I suspect that if we find bacterial mats (or soup) on Enceladus or Europa then it’s basically certain that life is everywhere. But we won’t even likely know that in my lifetime, so… I keep dreaming!


  • no, but they are often conflated

    femboy = a feminine boy, sometimes like the opposite to tomboy-- a gender presentation and/or aesthetic sense or style choice

    twink = an effeminate, small person, almost always referring to a man-- a description of body type and/or sexual dynamic

    these are not exhaustive definitions and are kind of reductive, actually… but as a quick casual explanation I think they mostly stand



  • Oh hey ugh I’ve been thinking about basically the same damn thing

    I’m also afab, trans masc, enby, pre-stuff, etc. I did martial arts for 13 years and only stopped because I moved away from my school. Kills me a little.

    The thing is, even when I was at the school I loved, I still had to grapple with disconnection between my gender identity and the way my perceived gender and sex interacted with the sport space. It’s not that they were mean or exclusive to women, it’s just that they inherently treated them a little different, and, well, my brain says I’m not a woman. Stop that.

    Right now I’m having the same problem because I live near the coast and I really want to get into spearfishing. It’s not that women are excluded, or even necessarily that they’re intentionally excluding queer or trans people, but there’s a hetero- and cis-normativity to these sport spaces that is so hard to penetrate.

    I’m sure I could ignore my own gender identity and ingratiate myself with other spearos the way I did before realizing I was non-binary-- usually by acting innocent, accepting lots of help, and talking in a sweet, high voice. Basically, if I play to their expectations of how “females” work I’m sure I’ll be included and eventually even respected. But… oh man do I not want to do that. And I can’t approach it the “male” way either, because it would be so jarring and odd that they’d think I was like… A bitch? Aggro? Etc.

    Uggghh anyway I don’t know how to help you (other commenter’s are doing a better job of affirming and encouraging) but let me provide the component of: yes I see you, yes I feel you, yes omg it sucks


  • I’m sorry! My knowledge of this process does not extend to the point where I could even give you a hint of the answer. To be honest, it would require me diving into the underlying mechanisms of your condition, and it sound like your doctor has said it isn’t even settled science why it’s happening, so I don’t think anyone can tell you if this would work for you.

    I know that isn’t what you wanted to hear, but two things: 1) this treatment is a long way off anyway, so anyone will have to wait for it to be available, and 2) there are probably many other treatments coming down the line for your condition… even if those also take a long time.

    Anyway, I’m sorry for your pain and that I couldn’t help! Honestly, I hope something will be available to help you many years before this becomes a treatment option.






  • That is so funny… tbh I know I’d get shit for this professionally, but it definitely frustrates me that we don’t allow people with few other choices to have access to crazy, left field treatment stuff.

    My best friend died of a specific and rare cancer this year. We know exactly how that cancer works on a molecular level, and we’ve found a few chemicals that interfere with the function of those cells in vitro while not seeming to harm average cells.

    Sure, it’s a huge risk to take that drug that’s only been tested in a dish, and it wouldn’t be worth it for most people. But he was going to (and did) die within a year of diagnosis. It’s not like he had other options.

    Maybe he should have invested in a rat costume ;)