A new biological rule?

Discussion:

(too old to reply)

jillery

2024-06-02 08:17:57 UTC

<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

RonO

2024-06-02 20:26:24 UTC

Permalink

Post by jillery
<https://dornsife.usc.edu/news/stories/rule-of-biology-centered-on-instability/>
<https://www.frontiersin.org/articles/10.3389/fragi.2024.1376060/full>
***************************
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

LDagget

2024-06-02 21:25:35 UTC

Permalink

It's a new term for me SAI. My initial reaction is that it seems like
an attempt to invent a general principle that is very aggressive
about collecting things to assertedly fit to that principle. So I'm
initially skeptical.

What are the more mundane ways to account for the key observations?

Taking the case of the rapid turn-over of mRNA, one more pedestrian
reasoning is that a cell wants to be synthesizing proteins based on
its current needs, not what its needs were 20 minutes ago. How can it
do so?

It can produce transcripts that it needs Now and have them somewhat
customized to degrade pretty soon, depending one the role, and then
just keep making more as the need persists. Or, it can have a secondary
mechanism to be triggered when the need ends to trigger something to
degrade specific mRNAs or block their translation.

Different types of function have different needs for temporal
sensitivity,
meaning the rate at which something gets turned off.

As it happens, there are all sorts of different pathways in play to
turn pathways off and on, and to destroy and recycle components. Some
types of systems are finely tuned like the G-protein receptors, getting
activated for a short burst of activity, sometimes extended slightly
by some cofactor or phosphorylation. But that theme has been so
successful that it has been copied and subverted to myriad pathways.

From my perspective, there seems to be a broad spectrum of solutions
that are cobbled together with a whatever works scheme along with
what could be considered to be frozen accidents, meaning some
regulation mechanism was "inherited" and so refined for some
derived function because evolution works with what it's got.

From that perspective, I don't see what this SAI does to improve on
how cell function and signal transduction works.

What I am tempted to see is a legacy from the first primordial cells,
and prebiotic chemical hypercycles, which I speculate were founded
upon rapid synthesis and turnover. That makes sense to me and places
everything within the context of systems that began with high potential
energy that functions as a engine which temporarily makes polymers
that help it temporarily make more while quickly recycling parts to
yet again make more. It becomes life when the processes become stable
enough, but it just keeps on with the rapid turnover. And for the
most part, that's what cells do.