Sujet : Re: A new biological rule?
De : rokimoto (at) *nospam* cox.net (RonO)
Groupes : talk.originsDate : 02. Jun 2024, 21:26:24
Autres entêtes
Organisation : A noiseless patient Spider
Message-ID : <v3ikhg$3erm7$1@dont-email.me>
References : 1
User-Agent : Mozilla Thunderbird
On 6/2/2024 3:17 AM, jillery wrote:
<https://dornsife.usc.edu/news/stories/rule-of-biology-centered-on-instability/>
Based on this cited article:
<https://www.frontiersin.org/articles/10.3389/fragi.2024.1376060/full>
From the abstract:
***************************
Rules of biology typically involve conservation of resources. For
example, common patterns such as hexagons and logarithmic spirals
require minimal materials, and scaling laws involve conservation of
energy. Here a relationship with the opposite theme is discussed,
which is the selectively advantageous instability (SAI) of one or more
components of a replicating system, such as the cell. By increasing
the complexity of the system, SAI can have benefits in addition to the
generation of energy or the mobilization of building blocks. SAI
involves a potential cost to the replicating system for the materials
and/or energy required to create the unstable component, and in some
cases, the energy required for its active degradation. SAI is
well-studied in cells. Short-lived transcription and signaling factors
enable a rapid response to a changing environment, and turnover is
critical for replacement of damaged macromolecules. The minimal gene
set for a viable cell includes proteases and a nuclease, suggesting
SAI is essential for life. SAI promotes genetic diversity in several
ways. Toxin/antitoxin systems promote maintenance of genes, and SAI of
mitochondria facilitates uniparental transmission. By creating two
distinct states, subject to different selective pressures, SAI can
maintain genetic diversity. SAI of components of synthetic replicators
favors replicator cycling, promoting emergence of replicators with
increased complexity. Both classical and recent computer modeling of
replicators reveals SAI. SAI may be involved at additional levels of
biological organization. In summary, SAI promotes replicator genetic
diversity and reproductive fitness, and may promote aging through loss
of resources and maintenance of deleterious alleles.
************************
AIUI there is a tension between stasis and diversity. During times of
environmental stability, it's advantageous to become increasingly
specialized to those static environmental conditions, which would
allow them to outcompete those less specialized. OTOH during times of
environmental instability, it's advantageous to develop multiple
random varieties aka genetic diversity, on the random chance that some
of those new varieties would be more fit to the new conditions, and
being more fit would naturally outcompete those less fit; no designer
required.
--
To know less than we don't know is the nature of most knowledge
It isn't stasis. They are talking about selective instability of cellular components. Their examples are RNA and protein. Obvious examples are the control of error rates in DNA replication, and the fine tuned gene regulation that is allowed because the mRNA transcripts have a certain half life, so transcriptional regulation can maintain functional levels of the viable transcripts and insure that specific levels of product are produced. During bacterial SOS mutation rate increases dramatically, and variants are produced that regulate the genes differently and change the function of the protein products. In the case of transcription, just think of how difficult it would be to regulate specific amounts of some protein product if the transcripts were viable for the life of the cell, and mRNAs in the egg cell persisted in the dividing cells throughout embryogenesis. You don't want those proteins made forever, but you only want them when they are needed.It takes a tremendous amount of energy to keep the transcriptional machiine running. Just think of the introns that are transcribed and then thrown away and recycled. Some genes like the DMD gene (Duchenne muscular dystrophe) that has a million base-pair transcript and all but 14 kilobase-pairs are thrown away. They think that the gene is so large because the time it takes to make a functional transcript is part of how the gene is regulated in terms of functional copies of the mature mRNA. Vertebrates with highly reduced genomes and smaller introns still have DMD genes over half a million base-pairs in length.If that is intelligent design, it is a really strange intelligent design. It looks like whatever worked was adopted. The designer could do anything, that is the major failure point for the ID scam. They claim that they can identify designer, design, but they obviously can't. Behe claims that the way that whales were designed is not how the designer would have done it (it is evolution by breaking things, that can be explained by Darwinian mechanisms), but no one is listening to him. All the IDiots seem to get out of Behe's stupidity is that whale evolution is a bad type of evolution. The evolution must have happened, but that never registers through the denial.
Ron Okimoto