#pseudogenic system

[your-fav-is-plural]

Gumball Watterson from the amazing world of gumball is a willogenic, pseudogenic and Borarogenic system ^^

Gumball Watterson from The Amazing World of Gumball is a Willogenic Pseudogenic and Borarogenic System!

Willogenic describes a system that was purposefully created or willed into existence, with no connections to tulpamancy

A Pseudogenic system is one that

a) A system created by them faking a system to the point the system became real

b) A system created by the self. Another term for parogenic

c) A reclamation of a term used against them

Borarogenic is an origin for (sisa)systems or headmates created out of boredom. It is under the parogenic umbrella

[the-ribombee-constellation]

Shout out to pseudogenic systems who faked being a system for so long they formed one! You're real and valid!

[ace-paradox]

Coining a -tive term I've been using.

Could not find a term that even remotely fit my experience, therfore I made a new one:

Faketive

A Faketive is a headmate who was pretended to be real before they became an actual member of the system.

This may include, but isn't limited to:

- Headmates initially pretended by a system who went on to become an acctual member of the system.

- Pretended headmates by singlets due to misunderstanding, curiosity, or external pressures to be a system.

- Headmates of Pseudogenic or Fakergenic systems

- Any Headmates with a source rooted in faking or lying about plurality.

- All headmates who feel they were once pretended by their headmate(s)

Faketives, recognizing their growth from a made-up identity to an acknowledged part of the system.

Related Terms:

Faketives may share characteristics with autojects, OCtives, or Mostives, especially when the fabricated identity originates within the system itself.

They may be related to roleplaytives or dramatitives if they were initially used to simulate scenarios or perform roles.

If stemming from an identity created under false pretenses (e.g., the system pretending to be someone else), they may align with Mendaxgenic origins.

Coined by me

requested by me

[sunflowersysalert]

Hello everyone!

︶⊹︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶

We are a pseudogenic and NOT PROUD sys!!

︶⊹︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶

BOUNDARIES

{ open to syscourse } { ask for discord in dms } { anti-endo dni } { proship dni }

︶⊹︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶

alter count: 50+

please ask questions about our sys!

our sys was made when we were 13

most of us are willogenic

︶⊹︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶

15 yrs old

host has unknown name \ doesn't want to disclose

they/them collectively

︶⊹︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶︶︶︶୨୧︶︶⊹︶

[sophieinwonderland]

how do you feel about the divide between the tulpamancy and the wider endo community? i keep seeing posts that wish for "more systems that piss people off" and list off obscure origins like firpergenic and pseudogenic, but not a mention of tulpas, even though we bear half of all the hate coming from sysmeds.

I see "pro-endo" posts that censor us as t*lpagenic, i see posts insisting that we have to leave our communities and start calling ourselves willogenic or other terms they came up with, otherwise we deserve to be the endos' scapegoats. i see posts from transplurals rejecting any mention of tulpamancy techniques that could help them and separating themselves from tulpamancy, even though i and i'm sure many others have had similar experiences of hating being a singlet and changing that with tulpamancy

Is this it? Is this all the discourse is ever going to be? I wish the kids would realise that they'll never win if they don't stick with their most controversial, and i wish we didn't have to defend both our own existence and theirs at the same time

I think the divide is overstated. There's a small handful of pro endos who are against the term tulpa. And they do tend to be rather vocal about it.

I mean, you do a search for "#pro endo #anti tulpa" in the tags and you'll see most are just people intentionally crosstagging to reach the other side. Tags are obviously not the only things that matter since not everyone tags their stuff as anti tulpa. But still, I just don't see this mentality that much outside of a very few pro endo blogs.

And at that, many of these anti-tulpa pro-endo blogs are people who have been in sysmed circles and picking up their talking points from them. Either "originally pro endo but fell into anti endo circles later" or "reformed anti endo who absorbed anti endo talking point before making the change but still doesn't accept tulpas."

You look into a lot of these so-called pro-endo anti-tulpas who make anti-tulpa posts, and it's not long until you find them arguing that endogenic and pro endo systems aren't oppressed and should shut up about it.

Or calling the pro-endo community nasty because we're not polite enough to people fakeclaiming our existences and harassing us for being plural for non-trauma reasons.

I would hardly call the "endogenic systems exist but I hate their community and think they should shut up about being oppressed" camp pro endo.

To the extent that actual anti-tulpa pro-endos do exist, I do find it's pretty stupid. I think it shoots yourself in the foot on multiple fronts. As you mention, it separates them from valuable resources that can help their systems.

It also plays into sysmed misinformation meant to divide the community. It's the same exact thing that happened when transphobes spread the talking point that "Faegender" was appropriative to sew division in the trans community, and demonize people for using neo pronouns.

The other thing is... tulpamancy is being researched right now more than other sorts of plurality, in a scientific way. When the Stanford Tulpa Study is published, it's going to be super important to spread that as much as possible.

And I expect we'll also see future studies on tulpas that will be into the actual creation process, which will be amazing. Imagine if we had a longitudinal study demonstrating that singlets can create headmates from scratch! This would completely and utterly destroy all remaining sysmed talking points.

Any pro-endo systems not sharing studies like this because they don't like a word would, frankly, be harming all endogenic systems with their silence.

But like I said, these tend to be a very vocal minority. I don't worry about them or concern myself with them.

I also think as tulpa studies come out and are the main evidence showing that plurality can be induced at any age into singlets, many of the stragglers will end up falling in line. 🤷‍♀️

[mleprae]

Yapping about leprosy's biology because I've yapped about everything BUT the bacteria itself

-

Leprosy is caused by 2 bacteria in humans; Mycobacterium leprae and Mycobacterium lepromatosis. The mycobacterium genus is a group of actinomycetota bacteria, the latter being known for their high guanine + cytosine content in their DNA and the former for their mycolic acid.

Bacteria are usually separated in two groups; gram positive and gram negative, positive bacteria have a thicker peptidoglycan layer, which is kind of like.. the 'skin' of a bacteria, while negative bacteria have a thinner peptidoglycan layer but they have an outer lipid wall that has lipopolyssacharides (LPS). LPS aids bacteria to recognize and bind to specific receptors, usually, a pathogen will be a gram-negative bacterias they are more adapted to recognize other cells but this isn't set in stone.

Mycobacteria however are neither of those, they have an outer wall that covers their entire body called 'mycolic acid', mycolic acid are long chains of fatty acids, these acids are what makes mycobacteria so resistant against many hostile enviroments and attacks, it's kind like bacteria armor! Other than that, mycobacteria also have very intricate mating rituals, some that can even look analogous to how us humans mate, this is importante, as bacteria of actinomycetota have high G+C content, meaning their DNA is less vulnerable to mutations and is more 'stable', these bacteria have evolved ways to still be very genetically diverse despite their circumstances.

Leprosy is the odd one of the group of mycobacteria, intracellular bacteria are a novelty (there's only very few species of bacteria that intracellular), and it seems to have went through a massive gene reduction event. Whatever happened to leprosy years ago, it made it into the second most genetically polluted bacteria, bacteria are very good at discarding useless junk genes that they don't need and most will only have 5% pseudogenes at MAX, so leprosy having 40% pseudo genes was a huge finding that left so many people confused.

One of those defective genes, seems to be some very important pathways (that's what we call a chemical chain event that leads to specific results, metabolism is a pathway, for an ex;) one of them, is the metabolization of carbohydrates. Carbohydrates such as sugar are the default energy for every living species, a species not being able to metabolize carbohydrate is unheard of, despite this, leprosy lacks the ability to do so; Or better yet, we can see that it still has its anabolic pathways of carbohydrates, but its's catabolism is missing. In other words, leprosy can break down carbohydrates, but it doesn't know how to use it.

So where does leprosy gets its energy? Well, lipids! Lipids are the nuclear energy of the body, it can story much more energy in a smaller space, and it releases much more than carbohydrate. The only reason why we don't use it, it's that breaking down lipids takes a long time. Lipids are still very important though, they usually become fat, which is just your body's energy storage. Leprosy is particularly found of triaglyceride (hence my little blog banner...), because it has fatty acids (few carbohydrates that it can use) and it's also a type of lipid.

All of this sounds like a disadvantage, but I promise you it's not !! Since leprosy enjoys colder spots, that are usually away from the bloodstream, it gets less nutrients, but it can live on fat alone so it doesn't need to risk itself to find a food source. The metabolism of fat also takes a long time, making leprosy a very slow grower, this helps the bacteria stay hidden and live for longer periods of times as;

A population of bacteria that eats too much will eventually drain it's nutrition source and quickly die off

A population of bacteria that grows too quickly will attract the attention of the immune system in it's weakest stage

As intracellular parasites, leprosy needs to parasitize a cell, it usually does this to a type of cell called 'Schwann cells', I'll take about these guys in a bit but first; the bacteria inside Schwann cells can force it to make more lipids and glucose, since leprosy does not know how to build glucose after it breaks carbs down, it needs a cell to do it for it. Schwann cells essentially become havens for the bacteria, sometimes, when leprosy is comfortable enough, these cells will be reprogrammed into another type of cell, carrying the bacteria inside it to somewhere else.

As for Schwann cells, they are cells that myelinate the peripheral nerves, nerves need to have extremely fast response and electrical impulses, the way they do this is- My god, ok, sorry, I'm going to have to explain biophysics to you ok?

Electricity is just a bunch of eletrons running around, there are many types of electrical currents, but the ones you need to understand are constant and alternating.

A constant is... well, a constant electrical current, the energy level is stable and there is no oscilation or change.

An alternating current however, is one where the eletrons are changing their direction really quickly, this leads to 'peaks' of electricity. A constant current is more stable, but an alternating current is much more faster and quick-responding, it's the one you use in electrical grids in houses and the ones our nerves uses!

Here's a graph for easier understanding.

Now neurons do this (kind of) by having a 'myelin sheath' which is made by the Schwann cells, the myelin sheath insulates the neuron while the nodes of ranvier (those little spaces between myelin sheaths) are the ones that do the job, electricity jumps from node to node increasing the speed and efficiency in how information is transmitted. It's a bit more complex than simple electrical currents, we call this type a 'saltatory' current, as it looks like energy is 'jumping from one place to another'

This is how leprosy causes numbness and fucks your nervous system, it destroys the Schwann cells that are responsible for keeping the neurons and the electrical current alive. An unmyelated neuron is MUCH slower in transmitting information than a myelated one, and although the former exist, they are usually very short and small to make up for it.

Here's an unmyelated nerve vs and myelated one.

As leprosy destroy more schwann cells, the neurons die, causing nerve thickness. Neurons find themselves to be very comfy inside the epineurium, which protects them and categorizes them into 'bundles' called fascicles. (Which in turn are protected by the perineurium)

What surrounds those little guys, is pretty much just conective tissue. As neuron dies, more connective tissue grows in their place in order to protect the other neurons from impact.

It's important to remember that the nervous system is an immunoprivileged system, which means that the immune cells are not allowed to enter. It does have it's own defenses, but they're not quite prepared to deal with leprosy, the immune cells there only weapon is phagocytosis- the act of eating a bacteria and letting your "stomach" acid kill it, but like I said, leprosy has bacteria armor; it doesn't affect it.

I would love to get into leprosy and the skin but it's 2 am. I need to sleep, and god help me write a text post on the 3 billion different cells types in the skin. good night!

[cleverwordsandotherstuffilike]

Medical innovations and scientific advances at Harvard Medical School through the decades (Part 2 of 2)

1995 Triple-organ transplant; kidney disease blood glucose levels

1996 How cells sense oxygen; Alzheimer's treatments; immune system advances

1997 p73 gene; aspirin

1998 Adult live-donor liver transplant

1999 Fluorescent molecular probes

2000 Brain abnormalities associated with abuse and neglect

2001 Circadian clock

2002 Rheumatoid arthritis pathway; C-reactive protein

2003 Multi-drug-resistant tuberculosis treatment; source of pre-eclampsia

2004 Blood stem cells; protein transfer

2005 Prenatal nutrition; herpes vaccine candidate

2006 Cholesterol mechanism; DNA sequencing techniques

2007 Cellular switch; rheumatoid arthritis gene; brown-fat cell switch

2008 RIPKI inhibitors; metastatic melanoma remission

2009 LIN28 protein; RNA interference; cancer cells' starvation; brown fat

2010 Enhancer transcription

2011 Kidney failure markers; cancer cell vulnerability; global health care budget models

2012 Tumour suppressor gene p53; ancient migration; infectious disease diagnostics

2013 Cardiac hypertrophy reversal; cathepsin k pathways

2014 Hematopoietic stem cells; pancreatic stem cells

2015 Bioartificial replacement limb; PD-1 pathway; The Lancet Commission on Global Surgery; pseudogene; damaged protein disposal; multiple sclerosis; somatic mutations; deafness gene therapies

2016 Sigma-1 receptor structure; Zika vaccine candidate; circadian rhythm-bipolar disorder link; microbiome

2017 Unlocking the blood-brain barrier; deciphering the structure of a scissor like enzyme

2018 The 'graying' of T cells; From one cell, a detailed road map

2019 Finding herpes' Achilles' heel; viral peptides critical to natural HIV control

2020 How COVID causes loss of smell; obesity fuels tumour growth; heart muscle dysfunction

2021 SARS-CoV-2 vaccine; immune evasion; AI gene interpretation; radiation vulnerability

2022 Fruit fly cell atlas; viral infection on video; boot camp for immune cells

2023 How the brain senses infection; new origin of breast cancer; the microbiome and cancer immunotherapy

[oh-okay-kay]

i think about this paper a lot. it discusses a *very* biological perspective (mainly through the lense of Ca2+ homeostasis and physiology), rather than a social perspective, on how gender differs from sex, and still comes to the conclusion that there are pretty much infinite genders, as well as occasionally discusses how being gay or bi or whatever is evolutionarily just as valid as being straight. super interesting

"It will be argued that it follows from the principles of Ca2+- physiology and homeostasis that all individuals of a sexually reproducing animal population have a personalized gender behaviour. Thus, subdividing gender-behaviours in hetero-, homo-, bi-, trans- etc. which all result from a differential use of the very same basic physiological principles, is too primitive a system that may yield false sociological interpretations."

"The logical, not to say self-evident answer given to: Why do many, in particular higher organisms produce sperm and eggs? usually is: That is the condition to have (chances for) a progeny and for being evolutionarily successful. Yet, this answer implies that testes and ovaries are aware of the reproduction-oriented drive the whole organism might have. This cannot possibly be the case: ovaries and testes do not plan for the future by producing gametes. According to the current status of evolutionary theory, there is no goal whatsoever in evolution."

"There is no generally accepted definition of gender, because the concept itself is not static but dynamic... the meaning of gender depends on who uses the word, in what context, and for what ends."

"If the reproduction-related behaviour would only be determined by the same set of genes that govern gonad formation and differentiation, there would probably only be heterosexuality and no homosexuality. But homosexuality, bisexuality, asexuality etc. do occur. Thus, the observed variability in behaviour must be caused by a more complex (set of) mechanism(s) than just the few genes that govern gonad differentiation."

"In such conditions, thus when gender behaviour becomes very personalized, the number of possible gender forms will near the number of all constituting individuals of the whole population. Thus in our own species there are as many different gender variants as there are individuals, 7 billion plus. But the total number of genes coding for proteins present in the human genome is only about 20,000. In addition, there are also some 10,000 pseudogenes, some genes can be subject to epigenetic modifications, and the junk DNA (that does not code for proteins) also has some regulatory functions. Even if all this is taken into account, the discrepancy 7 billion+ versus some 30,000+ genes and pseudogenes, illustrates that gender must have a physiological basis that enables a huge variability that can unfold while making use of only a limited number of genes."

"Because, many people believe that reproduction has been created or has come into existence with the goal of a progeny, gender variants that do not aim at a progeny, will be perceived as unnatural or, in a religious context, even as sinners. But reproductive archaeology teaches us that sexual reproduction did come into existence as the result of a sort of bacterial infection, not at all with the goal of producing a progeny in a novel way, namely by making use of special sex cells (sperm and eggs). Of course, heterosexuality is also in such a context a seemingly more successful form because it enables a progeny. However, this is a fortuitous coincidental feature, which does not imply any (in the case of humans) moral superiority: all gender forms have a cell-physiological basis. They are all variants of the same basic model. The supposedly better (in the long-term) form for the entire population, the heterosexual one, only seems better because it occurs in a much larger percentage of the population, and because most people erroneously think that the production of gametes and fertilization has come into existence in the course of evolution with the goal of producing a progeny."

"In conclusion: In this paper I advanced the physiology-based view that there are probably as many different gender variants as there are sexually reproducing individuals, and this not only in humans. Hence, there is no need to make subcategories in the gender variants with the purpose to install a moral hierarchy as they are all physiologically equal."

also, as an ace, the line "Thus in this view, sexual reproduction results from an evolutionary ancient bacterial-type infection, with sub-lethal effects. Thus it is a mild disease" is very funny

can’t stop thinking about my friend’s cishet partner who said last night that he doesn’t think anyone is the same gender. god-tier take.

[evoldir]

Fwd: Postdoc: UGent_Belgium.Two.PlantGenomeEvolution

Begin forwarded message: > From: evoldir@evol.biology.mcmaster.ca > Subject: Postdoc: UGent_Belgium.Two.PlantGenomeEvolution > Date: 11 January 2025 at 05:27:42 GMT > To: rdmpage@gmail.com > > > > > FWO-UGent funded bioinformatics postdocs - Unveiling the significance > of gene loss in plant evolution > > We are seeking two highly motivated postdoctoral researchers to join > our research team based in the Van de Peer lab, under the supervision of > Dr. Zhen Li, Assistant Professor at Ghent University/VIB Staff Scientist. > > The two positions are funded through an FWO research grant awarded to > Dr. Zhen Li and will focus on the evolutionary significance of gene loss > in shaping plant adaptation, speciation, and biological innovations. This > project aims to redefine our understanding of gene loss alongside gene > gain in plant evolution, focusing on developing novel genomic approaches > to analyze gene loss across diverse plant lineages and their evolutionary > consequences. To this end, the initial focus will be developing a novel > genomic approach integrating homolog identification and multiple genome > alignment to identify gene loss in plants and investigating its links > with species divergence and adaptive traits in various plant clades, > e.g., Orchidaceae, Poaceae, Solanaceae, Brassicaceae, and Fagales. > > Research Focus Areas > While the two positions will work closely together and share many > responsibilities, they have slightly different initial focus areas: > Position 1: Computational Genomics and Method Development > - Develop novel genomic frameworks for detecting gene loss in >  plant genomes > - Implement approaches to distinguish DNA deletion from pseudogenization > - Analysis of gene loss patterns across diverse plant lineages > - Explore graph-based algorithms for multiple genome alignment and >  ancestral karyotype reconstruction > > Position 2: Evolutionary Analysis and Network Biology > - Analysis of cross-species/-ecotype co-expression and gene >  regulatory networks > - Study of molecular mechanisms underlying how gene loss affects >  biological network rewiring > - Integration of phenotypic data with omics analysis > - Explore machine learning and network analysis methods > > We Offer > The VIB-UGent Center for Plant Systems Biology is a world-leading > science institution in Ghent, Belgium. Ghent University is among the top > 100 global universities according to several international rankings. > - A fully funded, full-time postdoctoral position for one year (with >  possibility of a two-year extension after positive evaluation) in a >  stimulating and supportive international research environment > - Access to state-of-the-art tools and computational infrastructure, >  including CPU/GPU clusters > - Opportunity to contribute to cutting-edge research in plant evolution >  and genomics > - Support for attending international conference and developing >  professional networks > - Comprehensive training in academic, technical, and career skills >  through VIB and Ghent University > > Motivated candidates are asked to apply online via the VIB application > procedure. > > A complete application file (English) should contain the following > documents: > - A cover/motivation letter (max. 2 pages) stating career goals, >  experience, and how these relate to your preferred position 1 and/or 2 > - A detailed CV, including a list of your scientific publications > - Contact information of at least two academic references > > For detailed information, please visithttps://jobso.id/ko16 > For inquiries about the positions, please mail to zhen.li@psb.vib-ugent.be > > Zhen Li

[leedsomics]

Solanum pan-genomics and pan-genetics reveal paralogs as contingencies in crop engineering

Pan-genomics and genome editing technologies are revolutionizing the breeding of globally cultivated crops. A transformative opportunity lies in the reciprocal exchange of genotype-to-phenotype knowledge of agricultural traits between these major crops and hundreds of locally cultivated indigenous crops, thereby enhancing the diversity and resilience of our food system. However, species-specific genetic variants and their interactions with desired natural or engineered mutations pose barriers to achieving predictable phenotypic effects, even between closely related crops or genotypes. Here, by establishing a pan-genome of the crop-rich genus Solanum and integrating functional genomics and genetics, we show that gene duplication and subsequent paralog diversification are a major obstacle to genotype-phenotype predictability. Despite broad conservation of gene macrosynteny among chromosome-scale references for 22 species, including 13 indigenous crops, hundreds of global and lineage-specific gene duplications exhibited dynamic evolutionary trajectories in paralog sequence, expression, and function, including among members of key domestication gene families. Extending our pan-genome with 10 cultivars of African eggplant and leveraging quantitative genetics and genome editing, we uncovered an intricate history of paralog emergence and evolution within this indigenous crop. The loss of an ancient redundant paralog of the classical regulator of stem cell proliferation and fruit organ number, CLAVATA3 (CLV3), was compensated by a lineage-specific tandem duplication. Subsequent pseudogenization of the derived copy followed by a cultivar-specific structural variant resulted in a single fused functional copy of CLV3 that modifies locule number alongside a newly identified gene controlling the same trait. Our findings demonstrate that paralog diversifications over short evolutionary periods are critical yet underexplored contingencies in trait evolvability and independent crop domestication histories. Unraveling these contingencies is crucial for translating genotype-to-phenotype relationships across related species. http://dlvr.it/TDDPht

[mbsintegratedmethod]

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[your-fav-is-plural]

Ame-Chan / K-Angel from needy streamer overload is Pseudogenic

Ame-Chan and K-Angel from Needy Streamer Overload are Pseudogenic!

A Pseudogenic system is one that

a) A system created by them faking a system to the point the system became real

b) A system created by the self. Another term for parogenic

c) A reclamation of a term used against them

[welcometotheneongarden]

Fakergenic:

Colors picked from r/SystemsCringe and r/FakeDisordersCringe's banners

Let's just say that the imperfections are on purpose (they aren't lol)

A reclaimed** origin label related to either

1) a headmate or sub/sidesystem formed by a system being fakeclaimed

2) a system/headmate/sub/sidesystem/etc that's origin is often seen as "fake" by others, it could be used on its own, or it could also be used alongside other origin labels (ie: fakergenic stressgenic, fakergenic endogenic, fakergenic multi origin, etc)

3) another term for pseudogenic (a system that formed after faking being a system)

4) a label used just to piss people who fakeclaim off (also like pseudogenic)

**reclaimed as in I saw a random comment on r/SystemsCringe that said it, that probably isn't the right word for what I'm trying to say, but hopefully this clears things up

Anyone can use our terms, because we (or atleast I) absolutely hate when people gatekeep theirs, but please don't interact outside of this post if you are anti endo!!!

Feel free to put this term on pluralpedia! /gen

[thecloudsys]

The cloud systems introduction !☁️

The body is 13, White, and Able-bodied (We mention this as some alters may be disabled)

We're a Multigenic/Mixed Origin system mainly of Tulpa, Traumaendogenic, Willogenic, and Pseudogenic.

We have 100+ alters and we're fictive&factive heavy!

We're friendly to any system of any origin.

This will be updated when we need/feel like it.

[solipsistful]

there’s something kinda funny in folks being like “i, someone very vocally and constantly anti-endogenic, told my therapist about endogenic multiplicity and they agree that it’s fake/dumb/mistaken”

cause like... i’m sure your introduction was very kind, the way you answer any question of “what is endogenic multiplicity?” with “it’s fake”

(like, i don’t doubt that therapists who don’t believe in multiplicity outside of the complex dissociative disorders exist. i just don’t think saying so-and-so therapist says so, therefore it’s real/fake isn’t particularly useful, given the 1) unprovability but more importantly 2) the extreme context-dependence of therapeutic interactions. i just mention our own therapist being ok more for the benefit of other non-DID/OSDD-1 systems who are worried about being slammed with a diagnosis if they were to come out. :V)

- Ace

[discoveringpmadupe]

The retrogene UTP14c, involved in human male infertility, ovarian cancer and the best way of studying it.

By; Palesa P. Madupe Literature survey So where does it all begin? Retrogenes, processed pseudogenes (PP) and pseudogenes are abundant in the human genome and most of their function was unknown up until recently (until the human genome project). They are mostly involved in disease development in humans, like in the case of myosin light chain kinase pseudogene which has been documented to be highly expressed in cancer cells (1). Pseudogenes are dysfunctional genomic loci with sequence similarity to functional genes but lacking coding potential due to the presence of disruptive mutations such as frame shifts and premature stop codons (2) . Pseudogenes are described into different categories; processed pseudogenes which are created via retrotranspositioning of mRNA from functional protein coding loci back into the genome, or duplicated unprocessed pseudogenes derived from duplication of functional genes or unitary pseudogenes, which arises through in situ mutations in previously functional protein coding genes (3) . Retrogenes are born via the reverse transcription of mature messenger RNA (mRNA) from parental genes and thus have no introns (mRNA sequence that can be converted into proteins) (4). They contain 3’ end poly A tail and are flanked by short directed repeats. They arise from transposable elements, defined as DNA sequences that have the ability to integrate into the genome at a new locus within the same cell. These elements contain DNA transposons and retrotransposons. Retrotransposons can be RNA that is reverse transcribed into DNA and then integrated into the genome at a new location (4). The original transposon is maintained in situ therefore it duplicates itself within the same cell; referred to as copy and paste method. Retrotransposons are devised into 2 classed based on the presence or absence of long terminal repeats (LTR). Those that contain LTRs are like retroviruses they contain them at both ends of the strand. The non-LTR have the 3’end poly A tails (5). The vast majority of retrotransposed copies of mRNA are inactivated into PP. It is only in a few cases that they evolve into new genes, ie. Retrogenes which can be transcribed and translated in to proteins. Like in the case of UTP14c gene; which is involved in 18S rRNA synthesis (the small subunit of the eukaryotic cytoplasmic ribosomes, which is essential in eukaryotic cells). The retrotransposed copy of the source gene is integrated into the 3’ un-translated region last exon of a glycerol transferase-containing gene (GT8). The 3’part of the exon 3 and the whole intron 3 and exon 4 of the GT8 gene are enlisted with unchanged exon-intron structure, to form a single intron containing UTP14c. This makes the exon segments of GT8 un translated (6). The source gene UTP14c is a ubiquitously expressed X-linked gene. In mouse; its retrogene UTP14b is expressed in the male germ cells and when its mutated it results in early spermatogenic arrest and male infertility (7). Humans have the strict ortholog of UTP14b in the synthetic region of chromosome 2, and it has degenerated and its no longer functional (it has become a PP). A second retrogene is found in chromosome 13 which is expressed in testis and ovaries the function has been documented to be equivalent to that of mouse UTP14b (6,8). The UTP14 protein has been predicted to be part of the small subunit processome complex that binds to U3 small nucleolar RNA involved in the synthesis of the 18S rRNA (9). The UTP14c gene has acquired specific promoter/enhancer elements, thus this restricts the activity of the gene in the ovaries and testis. The data machinery that is found in the germ cells is different from that is found in the somatic cells. Because the UTP14c gene is incorporated into the GT8 gene, this makes its production bypassed. The polyadenylation signal of the gene GT8 is lost (6). Mutations that occur within the UTP14c gene have shown to lead to early maturation arrest in the formation off sperm cells. The mutations lead to the protein of UTP14c gene not being able to form the protein complex of the synthesis of 18S rRNA. UTP14c is expressed in 50% of normal human ovaries and 80% of ovaries that have cancer (ovarian cancer). It was documented to down regulate tumour protein 53 (TP53) in both the nucleus and cytoplasm by targeting it for proteolytic degradation. This prevents the cancer cells expressing UTP14c from entering the apoptotic pathway. The loss of TP53 down regulates micro RNA-154 (miRNA-154) expression. This then activates factors that promote oncogenesis and cellular pluripotency which can develop ovarian cancer. How does expression of UTP14c actually disrupt the TP53 pathway? The TP53 regulates the expression of mi-RNA154, it binds to the promoter region of mi-RNA-154 and its up regulates the pre RNA synthesis of mi-RNA 154. It also bind to the muclear RNAse 3 drosha which stimulates the processing of the mi-RNA 154 pre- RNA into the mature version. The biological active form of mi-RNA 154 acts as an anti-tumorigenic factor blocking the expression of c-myc, cell reprogramming gene and the cells proliferation/invasion gene muc1 (6) . So how would we better study, UTP14c retrogene? A little bit of history Recombinant DNA technology (10) has changed how we understand the functioning of genes, proteins and nucleic acid. Recombinant DNA technology refers to making of new combinations of DNA fragments which are not found existing together in nature. The isolation of the desired DNA segments allows for exact DNA analysis, and practical application in medicine like drug discovery, in agriculture like the creation of bio-control agents and in industrial application production of food additives. Here is an oversimplified way of making recombinant DNA; isolate DNA from whatever source, cut with restriction enzymes, ligate (essentially paste) into cloning vector, then transform the recombinant DNA molecule into host cell, grow the host. Each cell from then onwards will carry the desired recombinant DNA molecule. Each of the steps mentioned here have intrinsic and extrinsic factors to them and their not as plain as mentioned. To further study the recombinant DNA molecule, depends on what the researcher is interested in. To determine the function of the recombinant DNA molecule one can conduct a site generated mutagenesis, the recombinant DNA fragment may be changed by changing a base in the primer sequence, for the polymerase chain reaction (PCR) of the cloned DNA molecule. During the PCR the amplicons generated will contain the mutation selected for by the researcher (11). Because of the generated site mutation the gene produce for that DNA fragment might not function like the wild type gene, thus one can then extrapolate that a mutation at position X leads to noticeable missing functions. More recently we have seen outbreaks of the combination of recombinant DNA technology and nanoscience. Nanoscience refers to the science; manipulation and the development of chemical and biological structure that are on the scale of single atoms. Like in the production of antibodies, this technology is been used to manufacture antibodies that have very high affinity to specific substrates. The problem has been a way of delivering these antibodies to that specific site. Ingestion would lead to the immune system attacking them. The attachment of these recombinant antibodies to carbon nanotubes with radio or fluorescent labelling, can directly deliver antibodies directly where their required (12). Recombinant DNA technology has also advanced the study of protein function and drug design. Knowing the three-dimensional (3-D) structure of a protein has enable the determination of the active site (where substrates bind) in vivo. Knowing the active sites of protein and enzyme has enabled drug design to be more effective (13). The 3-D structure of proteins can be determined via nuclear magnetic resonance (NMR) spectroscopy, which is able to reveal atomic structures of macromolecules in solution. NMR relies on the fact that atomic nuclei are magnetic. The purified protein in solution is then placed in a strong magnetic field and probed with radio waves. A distinct resonance is observed and that can be analysed to give a list of atomic nuclei that are close to one another, and to characterise the local conformation of atoms that are bonded together. All these specifications are used to a model a protein (14). Protein X-ray crystallography, it’s the determination of the 3-D structure of biological macromolecules using diffraction technology on a single crystal. This technique is much better than NMR because X-ray crystallography gives a better/ high resolution. The first protein crystal structure was of myoglobin in the year 1932 by Theorell A, the resolution of the protein was 6 Å (Angstron). Resolution measures the amount and level of details present in the protein. High resolution structure are those that have very low Angstron values < 2 Å. For this method the protein is purified and crystallised and the hit with intense beam of X-rays. The diffraction is measured and then analysed to determine the distribution of electrons in the protein (15). X-ray crystallography provides detailed atomic information, showing every atom in the protein together with atomic details of ligands, inhibitors, ions, and other molecules that incorporated in the protein. With the backdrop of this information the best way of understanding the structure and function of the UTP14 protein is via recombinant DNA technology and X-ray crystallography, especially if we want to eventually design a drug that can be used in fighting the cancer and infertility that is caused by the UTP14c gene. Citations 1. ​Han YJ, Ma SF, Yourek G, Park Y-D, Garcia JGN. A transcribed pseudogene of MYLK promotes cell proliferation . FASEB J. 2011; 2. ​Mighell AJ, Smith NR, Robinson PA, Markham AF. Vertebrate pseudogenes. FEBS Lett. 2000; 3. ​Harrison PM, Zheng D, Zhang Z, Carriero N, Gerstein M. Transcribed processed pseudogenes in the human genome: An intermediate form of expressed retrosequence lacking protein-coding ability. Nucleic Acids Res. 2005; 4. ​Kaessmann H, Vinckenbosch N, Long M. RNA-based gene duplication: Mechanistic and evolutionary insights. Nature Reviews Genetics. 2009. 5. ​Ding W, Lin L, Chen B, Dai J. L1 elements, processed pseudogenes and retrogenes in mammalian genomes. IUBMB Life. 2006. 6. ​Rohozinski J, Lamb DJ, Bishop CE. UTP14c Is a Recently Acquired Retrogene Associated with Spermatogenesis and Fertility in Man1. Biol Reprod. 2005; 7. ​Boettger-Tong HL, Johnston DS, Russell LD, Griswold MD, Bishop CE. Juvenile Spermatogonial Depletion (jsd) Mutant Seminiferous Tubules Are Capable of Supporting Transplanted Spermatogenesis1. Biol Reprod. 2005; 8. ​Bradley J, Baltus A, Skaletsky H, Royce-Tolland M, Dewar K, Page DC. An X-to-autosome retrogene is required for spermatogenesis in mice. Nat Genet. 2004; 9. ​Dragon F, Gallagher JEG, Compagnone-Post PA, Mitchell BM, Porwancher KA, Wehner KA, et al. A large nucleolar U3 ribonucleoprotein required for 18S ribosomal RNA biogenesis. Nature. 2002; 10. ​Cohen SN, Chang AC, Hsu L. Nonchromosomal antibiotic resistance in bacteria: genetic transformation of Escherichia coli by R-factor DNA. Proc Natl Acad Sci U S A. 1972; 11. ​Hemsley A, Arnheim N, Toney MD, Cortopassi G, Galas DJ. A simple method for site-directed mutagenesis using the polymerase chain reaction. Nucleic Acids Research. 1989. 12. ​McDevitt MR, Chattopadhyay D, Kappel BJ, Jaggi JS, Schiffman SR, Antczak C, et al. Tumor Targeting with Antibody-Functionalized, Radiolabeled Carbon Nanotubes. J Nucl Med. 2007; 13. ​Verlinde CL, Hol WG. Structure-based drug design: progress, results and challenges. Structure. 1994; 14. ​Wüthrich K. The way to NMR structures of proteins. Nat Struct Biol. 2001; 15. ​Wlodawer A, Minor W, Dauter Z, Jaskolski M. Protein crystallography for aspiring crystallographers or how to avoid pitfalls and traps in macromolecular structure determination. FEBS J. 2013;