Shining light on the pathways that give rise to pluripotent cells in rodents and primates

Unpacking embryonic pluripotency
Blastocysts in this study were immunostained to show pluripotency factor NANOG localised to the inner cell mass, primitive endoderm specifier GATA6, outer trophectoderm marker CDX2 and nuclei. Credit: Original figure by Bertone and colleagues adapted by Spencer Phillips, EMBL-EBI

Researchers at EMBL's European Bioinformatics Institute (EMBL-EBI) and the Wellcome Trust- Medical Research Council Cambridge Stem Cell Institute at the University of Cambridge have identified factors that spark the formation of pluripotent cells. Their findings, published in Developmental Cell, shed light on human embryonic development and help research into cell reprogramming and assisted conception.

Embryonic are widely known for their ability to differentiate into any cell type - a state called pluripotency. This state is short lived in the embryo, but is essential to normal development. In this study, the researchers mapped when and where genes were expressed (turned on or off) during of the mouse and common marmoset, a nonhuman primate species. This allowed them to pinpoint changes that regulate pluripotency in both mammals. They analysed the complex network of gene regulation that supports pluripotency, looking closely at how this network comes together and later collapses as cells exit the pluripotent state to become specialised cell types.

"Our goal was to generate a comprehensive map of gene expression in the early stages of embryogenesis in the mouse, which has traditionally been the best model for mammalian development, and to see how that knowledge could be translated to primates," explains Paul Bertone, former EMBL-EBI group leader now at the Wellcome Trust-MRC Stem Cell Institute.

To compare in rodents and primates, the researchers used single-cell RNA sequencing on small clusters of cells (8-20 cells) to establish precise gene-expression patterns for specific stages of early development. The results provide a framework for understanding the emergence and progression of pluripotency in different mammals.

"Many of the genes that give rise to the pluripotent identity in mice were also expressed in marmoset, demonstrating a common foundation for pluripotency in mammals," says Austin Smith, also of the Stem Cell Institute. "But there were some differences in signalling pathways between the two species, indicating that lineage specification in primates is not entirely conserved."

"We found that WNT signalling in the marmoset is critical for normal differentiation of one of the first three cell lineages to emerge," Paul continues. "Inhibiting this pathway has a profound effect - one of those lineages is subsumed by pluripotent cells rather than forming correctly. It will be interesting to see through in vitro studies whether WNT and perhaps other pathways are similarly utilised in humans."

This highly interdisciplinary study blends traditional embryology, genomics and bioinformatics. The result is a valuable resource for identifying the factors and pathways that regulate pluripotency in different mammals. The findings can also be used to optimise embryonic stem-cell derivation, and reprogramming to pluripotency, in cell cultures. The knowledge gained helps researchers understand early lineage decisions in embryonic , potentially leading to improved methods for human blastocyst for assisted conception.


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More information: Thorsten Boroviak et al. Lineage-Specific Profiling Delineates the Emergence and Progression of Naive Pluripotency in Mammalian Embryogenesis, Developmental Cell (2015). DOI: 10.1016/j.devcel.2015.10.011
Journal information: Developmental Cell

Citation: Shining light on the pathways that give rise to pluripotent cells in rodents and primates (2015, November 9) retrieved 22 September 2019 from https://phys.org/news/2015-11-pathways-pluripotent-cells-rodents-primates.html
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JVK
Nov 09, 2015
Excerpt: "This highly interdisciplinary study blends traditional embryology, genomics and bioinformatics."

My comment: Nutrient-dependent RNA-mediated gene duplication and RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all living genera link what is currently known about physics, chemistry, and biology via the conserved molecular mechanisms that blend epigenetically effected transgenerational inheritance of morphological and behavioral phenotypes with what is known about embryology, genomics and bioinformatics.

Taken together the links from atoms to ecosystems make it perfectly clear that protein folding is biophysically constrained and that RNA-mediated events link ecological variation to ecological adaptation via metabolic networks and genetic networks manifested in the context of supercoiled DNA that protects organized genomes from virus-driven genomic entropy.

JVK
Nov 09, 2015
Journal article excerpt: "These results highlight metabolic differences, in particular with regard to amino acid biosynthesis, between the mouse and marmoset embryo."

The differences in amino acid biosynthesis lead to differences in protein biosynthesis and degradation during thermodynamic cycles that must lead to organism-level thermoregulation.

Nutrient-dependent organism-level thermoregulation links the epigenetic landscape to the physical landscape of DNA in species from microbes to humans via their pheromone-controlled physiology of reproduction, which leads to ecological speciation and all biodiversity.

For other examples see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model http://www.ncbi.n...24693353

Nov 10, 2015
ncbi.n...24693353
For better and more accurate scientific information, see: Criticisms of the nutrient-dependent pheromone-controlled evolutionary model.
http://www.ncbi.n...4049134/


JVK
Nov 10, 2015
The "Criticisms" of the biologically uninformed science idiot Andrew Jones, did not address the atoms to ecosystems model of RNA-mediated cell type differentiation. The criticisms were like a tantrum displayed by someone who screams "I DON'T LIKE YOUR MODEL" and hates the fact that there is no other model of biologically-based cause and effect.

Biologically-BASED cause and effect starts with base pair changes.

See the parody that links energy-dependent base-pair changes to cell type differentiation in all living genera via what is known to serious scientists about how supercoiled DNA protects organized genomes from virus-driven entropy.

https://www.youtu...youtu.be All About that Base (Meghan Trainor Parody)

See also: Structural diversity of supercoiled DNA http://www.nature...440.html

Nov 10, 2015
youtu.be
Spamming with a youtube video doesn't validate your claims
See the parody that links
the parody doesn't "link" anything except for your annoying habit of spamming the site with irrelevant youtube video's and the trolling nature of your comments
The criticisms were like a tantrum
the criticisms were valid reputable science validated by experimental evidence and repetition therefore it conformed to the scientific method and refuted your claims

you have a history of being a chronic liar on this site, whereas ANON has a history of valid claims supported by evidence

why should anyone believe you, especially when you actively support a religion known to publish pseudoscience?

JVK
Nov 10, 2015
See: http://www.las.il...dex.html

why should anyone believe you


Thanks for asking.

People should believe me because I published a series of review articles that link RNA-mediated cell type differentiation in species from microbes to man via the conserved molecular mechanisms that link nutrient-dependent amino acid substitutions and the physiology of reproduction to protection against virus-driven genomic entropy in the context of everything currently known about supercoiled DNA.

The alternative is to believe the pseudoscientific nonsense touted by biologically uninformed science idiots who are still trying to link mutations to the evolution of increasing organismal complexity outside the context of biophysically constrained RNA-mediated gene duplication and the RNA-mediated stability of organized genomes.

ANON has a history of valid claims


Andrew Jones (aka ANON) is a biologically uninformed science idiot.

Nov 11, 2015
People should believe me because I published a series of review articles
@jk
1- argument from authority logical fallacy: you are not capable of providing evidence for your claims therefore your claims are called "opinion" at best, but usually just "false claims"
http://www.auburn...ion.html

2- an article is not a study

3- you have also published derogatory and libelous claims about other respectable researchers who are pioneers in their field

4- you have also published fraudulent claims that are considered felonious

5- you have also been proven, on this site alone, to be a chronic liar as well as creationist proselytizer, therefore any claim you make is suspect unless there is validating information

there is no reason anyone should trust you to do anything
especially that requiring credibility
and all this due to your posting history here on PO alone

Nov 11, 2015
@jk cont'd
the above is also called a False Authority fallacy
The alternative is to believe the pseudoscientific nonsense
argument from stupidity, the evidence states that you are wrong, therefore the logical conclusion is that you are wrong
there is no evidence that you've provided that substantiates that people who believe in the Theory of Evolution believe in pseudoscience (this is called a False Claim because the evidence supports Evolution and not your claims)

so what you are doing is attempting to shame people into following you, or use fear based arguments into accepting your perspective
this is called RELIGION, not science

in science, there is evidence, and then validated evidence

you can't supply either as the bulk of your arguments are: ad hominem, circular reasoning, argument from ignorance, red herring, repetition (especially of blatant false claims) or argument from (personal) incredulity

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