Understanding the Stem Cell Niche

Description: Stem cells provide an attractive model to study human physiology and disease. However, technical challenges persist in the biological characterization and manipulation of stem cells in their native microenvironment. The Scientist brings together a panel of experts to discuss interactions between stem cells and external cues, and the role of the stem cell niche in development and disease. Topics to be covered include the molecular mechanisms of hematopoietic stem cell niche interactions and techniques for engineering 3-D stem-cell microenvironments.

My comment: The stem cell niche links ecological, social, neurogenic, and socio-cognitive niche construction via nutrient-dependent RNA-mediated protein folding chemistry that biophysically constrains cell type differentiation in all cells of all individuals of all species until viruses accumulate and over-ride the innate immune system that protects all organized genomes from virus-driven entropy.

PLOS Genetics Research Prize 2015: Winner Announced

My comment: The winners of this prize failed to link anything known about nutrient energy-dependent prevention of virus-driven genomic entropy. They placed what is known to serious scientists about cell type differentiation into the context of mutation-driven evolution in E.coli. The winners ignored biophysically constrained RNA-mediated protein folding chemistry.

Brief mention is made of the fact that clonal interference “…has recently been inferred to be an important determinant of the evolution of the influenza virus [14].” The “inference” is accepted and this fact is ignored.

FACT: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.

Instead of linking nutrient-dependent receptor-mediated changes in protein folding chemistry from ecological variation to ecological adaptations in gut microbes, the authors linked mutations to differences in E. coli that “evolve” in two days — despite no evidence that mutations are fixed in the organized genomes of any population of any species on Earth. Amino acid substitutions that differentiate all cell types of all individuals are fixed in species via the physiology of reproduction.

Congratulations to PLOS Genetics for rewarding research that continues to misrepresent everything known to serious scientists about biologically-based cause and effect because the researchers framed their results in the context of ridiculous neo-Darwinian pseudoscientific nonsense.

See for comparison:  Structural basis for leucine sensing by the Sestrin2-mTORC1 pathway


Eukaryotic cells coordinate growth with the availability of nutrients through mTOR complex 1 (mTORC1), a master growth regulator. Leucine is of particular importance and activates mTORC1 via the Rag GTPases and their regulators GATOR1 and GATOR2. Sestrin2 interacts with GATOR2 and is a leucine sensor. We present the 2.7-Å crystal structure of Sestrin2 in complex with leucine. Leucine binds through a single pocket that coordinates its charged functional groups and confers specificity for the hydrophobic side chain. A loop encloses leucine and forms a lid-latch mechanism required for binding. A structure-guided mutation in Sestrin2 that decreases its affinity for leucine leads to a concomitant increase in the leucine concentration required for mTORC1 activation in cells. These results provide a structural mechanism of amino acid sensing by the mTORC1 pathway.

See also:  Oscillatory stress stimulation uncovers an Achilles’ heel of the yeast MAPK signaling network


Cells must interpret environmental information that often changes over time.

My comment: The information is linked from nutrient-dependent metabolic networks to genetic networks and pheromone-controlled feedback in yeasts that links the biophysically constrained nutrient-dependent pheromone-controlled physiology of reproduction across all species via the conserved molecular mechanisms of RNA-mediated protein folding chemistry.

See also: Chromatin Unfolding by Epigenetic Modifications Explained by Dramatic Impairment of Internucleosome Interactions: A Multiscale Computational Study


This molecular level description of the effect of histone tails and their charge modifications on chromatin folding explains the sequence sensitivity and underscores the delicate connection between local and global structural and functional effects. Our approach also opens new avenues for multiscale processes of biomolecular complexes.

See also: the molecular epigenetics section of our 1996 Hormones and Behavior review: From Fertilization to Adult Sexual Behavior.  Help to stop the pseudoscientific nonsense touted by neo-Darwinian theorists before they lead to the death of us all by preventable genomic entropy.

MORE RECENT NEWS about RNA-mediated cell type differentiation:

Altering RNA helicases in roundworms doubles their lifespan: similar technique could be used on human cells, experts say

Hummingbirds rely on raw power, not physique, to outmaneuver rivals

Living in thin air: Fruit fly research pinpoints genomic hallmarks of human high altitude adaptation

‘Death Clock’ In Cells Can Tell Doctors When Patients Will Develop Cancer

Our closest wormy cousins: About 70% of our genes trace their ancestry back to the acorn worm

Neural circuitry feeding into the lateral hypothalamus

My comment: If you do not understand the fact that RNA-mediated cell type differentiation links every aspect of what was recently reported in these articles, start asking questions.  I’ve encouraged discussion here and on my FB group but few people seem willing to comment. I think they are afraid to upset those who are touting pseudoscientific nonsense and teaching their ridiculous theories to another generation of researchers who will become biologically uninformed science idiots who cannot link atoms to ecosystems, which is what serious scientists do.

Keep Reading