Logic and evolution (Introduction)

by David Turell , Tuesday, July 26, 2016, 23:23 (3043 days ago) @ dhw

DAVID: I would note that cells can only react with their available molecular reactions that are onboard, which in your view may well be God given, and I agree.
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> dhw: My view is that their autonomous intelligence may well be God-given (50/50), and I would not define intelligence as “their available molecular reactions”.-
I have a new study that defines these molecular and gene controls over cell division. Note the headline which uses the word 'decision' and feedback loop:-http://phys.org/news/2016-07-nota-cellular-feedback-loop-enables.html-"New research from the laboratory of Professor Bruce Stillman, Ph.D., president of Cold Spring Harbor Laboratory (CSHL), sheds light on a critical decision that every newly born cell makes: whether to continue to proliferate or to exit the cell-division cycle.-" The decision to stop proliferating depends on delaying the expression of a protein called Cyclin E. Cyclin E and its partner, protein kinase CDK2, are key regulators of the decision of whether a cell will commit to a new round of cell division or remain in a non-proliferative state. Stillman and postdoctoral investigator Manzar Hossain, Ph.D., today publish in eLife the results of experiments demonstrating precisely how Cyclin E expression is kept in balance in normal cells by the opposing actions of two proteins.-"The two proteins are called ORC1 and CDC6. As Stillman's lab showed last year, during mitosis, when two daughter cells separate, each inherits chromosomes to which ORC1 is bound. Thus it is inherited into the new cells and can immediately act to control Cyclin E levels. Previously, the lab had shown that when ORC1 is missing, Cyclin E levels rise.-"Now, Stillman and Hossain have discovered that ORC1 represses the activation of the gene (called CCNE1) that encodes instructions for manufacturing Cyclin E. This means that as the next cell cycle begins—a phase biologists call G1—Cyclin E initially is not expressed because ORC1 blocks the CCNE1 gene.-"The new research reveals how ORC1's anti-proliferative role early in the life of a new cell is part of a feedback loop whose pro-proliferation member is the ORC1-related protein CDC6, another important DNA replication factor.-"'If cells integrate signals from their environment that promote another round of cell division, a pathway is engaged, in which a complex formed by Cyclin D and CDK4 (a cyclin-dependent protein kinase) triggers a cascade of effects that culminate in amplification of the cell's commitment to cell division," Hossain explains. The mechanism behind this amplification involves an interaction between Cyclin E-CDK2 and CDC6. Their level in the cell, in turn, is regulated by a transcription factor called E2F, which itself is controlled by a tumor suppressor protein called RB and an enzyme that adds methyl groups to histone proteins, called SUV39H1.-"Hossain and Stillman report that early in the newly born cells, ORC1 is present at the promoter element of the gene that encodes Cyclin E, at which position it interacts with the RB protein and SUV39H1. The interaction results in repression of E2F-dependent transcription of the Cyclin E-encoding gene. Later in the G1 phase of the cell-division cycle, as cells receive signals that they should proliferate, CDC6 cooperates with Cyclin E and its protein kinase partner CDK2, to biochemically counter this repression, thus acting to dramatically increase the expression of the gene that encodes Cyclin E. This amplification process contributes to committing the cell to a new round of DNA duplication and chromosome segregation. Thus a feedback loop is established in which one DNA replication protein, CDC6, antagonizes the repressive action of another DNA replication protein, ORC1. (my bolds)-***-"The opposing effects of ORC1 and CDC6 in controlling the level of Cyclin E thus contributes to the stability of the genome," Stillman says. "It is a mechanism for directly linking the process of DNA replication with a cell's commitment to divide.'" -Comment: This all sounds very automatic and controlled to me. The only part of the reactions that might fit the issue of conscious action or 'thought' is the role of the genes in these reactions, what proteins they code for, and whether the gene is repressed in transcription or increased in expression by these molecular relationships. We know genes code for protein production, but how they might be exerting other influences is not yet discovered. Note that the molecules themselves increase or decrease gene function!