If you know someone who has linked differences in the energy of photons from the proton motive force to the physiology of reproduction and all biophysically constrained biodiversity, ask if they will attend Schrödinger at 75-The Future of Biology
For contrast, touting genetic evolution is not the future of biology.
Understanding the forces that shape genetic evolution is a subject of fundamental importance in biology and one with numerous practical applications. Modern experimental techniques give insight into these questions, but inferring evolutionary parameters from sequence data, such as how an organism’s genotype affects its fitness, remains challenging. Here we present a method to infer selection from genetic time-series data using a path integral approach based in statistical physics. Through extensive numerical tests we find that our method exceeds the current state of the art in the successful classification of mutations as beneficial or deleterious in a variety of scenarios, while also yielding orders of magnitude improvements in run time. Our approach can also be extended to jointly infer other evolutionary parameters such as the effective population size and mutation rates.
Serious scientists do not infer evolutionary parameters using sequence data. They link natural selection for energy-dependent codon optimality to biophysically constrained viral latency. Virus-driven energy theft is linked from mutations to all pathology. There is no such thing as a beneficial mutation.
During a cell cycle, cells grow and divide. Recent single-cell experiments show that gene expression levels depend on the cell cycle. Particularly important is the proportion of the number of mRNA and protein to the cell volume. It is not clear how cells maintain a constant mRNA and protein concentration as the cells grow. Here we propose a coarse-grained gene expression model incorporating ribosomes and RNA polymerases, which captures the exponential growth of mRNA and protein number. We show that the homeostasis of mRNA and protein concentrations during the cell cycle can be achieved in a robust manner independent of cell shape. Furthermore, we show that the fluctuations in ribosome and polymerase numbers do not propagate to protein concentrations while the fluctuation in cell density does. Furthermore, our model reconciles the discrepancy between the experimentally observed negligible correlations between mRNA and protein levels, and the predicted positive correlations from previous models
Energy-dependent changes in the microRNA/messenger RNA balance have been linked from RNA-mediated cell cycles to gene expression in more than 70,000 published works. See: microRNA
See also: Applications of ligation-mediated PCR
A nick in a strand is any place where there’s a missing covalent bond between a sugar and the next adjacent phosphate. Nicks can arise from DNA damage, during normal DNA replication, or from the action of nuclease enzymes. Since a nick breaks the continuity of the backbone of one strand, it must be repaired by re-forming the missing covalent bond in order to make the DNA molecule intact again. This job of sealing nicks (specifically, nicks that occur between a sugar 3′ -OH group and the adjacent phosphate attached to the preceding sugar’s 5′ -OH group) is the function of DNA ligase. Using a molecular energy source (which differs depending on the enzyme source organism), DNA ligase reforms the missing covalent bond and the strand is whole again. Two aspects of this are critical:
The nick to be repaired occurs on a single strand but in the context of a double-stranded molecule.
The bases of the nicked strand, and particularly those directly flanking the nick site, must be properly base-paired to the opposite (un-nicked) strand.
It’s not hard to imagine why this is: the base pairing is required to hold the two parts (sugar 3′ -OH and the next phosphate) in place for the ligase enzyme active site to catalyze joining them. If either one of these isn’t base-paired down and is flopping about with thermal motion, the reaction geometry doesn’t occur, and no new bond can be made.
Simply put: It’s all about that base and energy-dependent RNA-mediated DNA repair.
If you are still trying to put what is known about DNA repair and cell type differentiation back into the context of neo-Darwinian evolution, you are not a winner.
Nobody wants to belong to the party of losers. One of the best strategies in such a case is evidently an interpretation of the change as a gradual accumulation of knowledge while their work has always been at the cutting edge. — Kalevi Kull
See also: The spread of true and false news online
Additionally, the article’s authors point out that false information affects not only the political sphere but also areas not previously regarded as political, such as public health topics like nutrition and vaccinations, as well as the stock market.
Do you know someone who has consistently touted the use of vaccinations compared to nutrition? Are they paid to do that or are they biologically uninformed?