#ken weiss

[orange-wedges-blog1]

Psychedelic Burlesque, this is the Greatest Show on Earth Photos by Jay Goode, Drawings by Sierra Bandit Photo Collage by Ken Weiss & Bruce Tobin (The East Village Other, March 29 - April 4, 1968)

[bobnorthway]

Models and learning in ‘complex’ biological systems: the need for new conjectures and a more sophisticated realism

Models and learning in ‘complex’ biological systems: the need for new conjectures and a more sophisticated realism

Models and learning in ‘complex’ biological systems: the need for new conjectures and a more sophisticated realism May 21, 2016 

I am not the first to comment on the significance of a recent essay by Robert Epstein entitled “The empty brain” in Aeon magazine. (For other comments see e.g. Ken Weiss in his ecodevoevo blog on May 19th [1]). In his essay Epstein strongly argues that the human brain…

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[diyeipetea]

Entrevista con Paul Bley: el pianista integral, segunda parte

Segunda parte de la entrevista a Paul Bley que el pasado 28 de octubre de 2008 realizaron Ken Weiss (Jazz Improv Magazine) y Nobu Stowe (Jazz Tokyo). El cuestionario fue realizado con aportaciones de Nobu Stowe, Ken Weiss, Kenny Inaoka (Jazz Tokyo) y Pachi Tapiz (Tomajazz). Un agradecimiento especial a Mark Christman (Ars Nova Workshop)…

Entrevista con Paul Bley: el pianista integral, segunda parte was originally published on Tomajazz 2.5

[biochemistries]

While population genetics is very useful for putting some plausibility brackets around interpretations of genetic data from populations, it is still largely a one-gene-(or one linkage group of genes)-at-a-time theory; that is, it doesn't concern itself with actual traits or how they are manifest, and so on. Indeed, leading developmental geneticists have, rightfully in our view, complained about the self-proclaimed theory of evolution's omission of the way that actual organisms are assembled, and evolve, and the role genes play in that. ...You may not be old enough to remember the phrase 'beanbag genetics' but it symbolized the naturalist's view that whole organisms or even ecosystems need to be studied as interaction entities, rather than trying to understand evolution by particularizing things down to individual genetic variants, even if the latter are an essential part of the story. That sort of reductionism was missing the point. But have we long ago learned that lesson? In fact, today's Big Data GWAS-y world is conceptually still largely wedded to beanbag genetics. It is still driven by a reductionistic approach that essentially believes that by enumerating the individual beans in each person's genome, that person's entire nature can be understood or even predicted from the moment of conception. Is this too much of a simplification or overstatement? Is there a reason other than molecule-worship that the stress is so heavily on individual, particulate entities like 'genes', even though we know the genome is far from so clearly discretized in function? Look past the caveats and denials offered by the Big Data empire to what they they are mainly doing, look at how they bury or pass over their caveats, and judge for yourself. Effort is being made by people to study 'systems', such as molecular interaction networks. This is a recognition of the problem posed by hyper-reductionism. It is a step in a good direction, but even the systems approach largely seems beanbag in nature, by approaching complex traits as if they were a beanbag of internally interacting systems that can be enumerated and treated as units. Network interactions are obviously relevant and involved in biological organisms, but it is not so clear, to us at least, that that path will be the best one to understand complex traits sufficiently well. At least, systems approaches force us to consider interactions among components as fundamental to life.

Ken Weiss, Are we still doing 'beanbag' eu(genetics)? Part I. Some history. December 15 2014

Way back in 1964, a famous paper was published in Perspectives in Biology and Medicine (vol 7: 343-359, and reprinted in the International Journal of Epidemiology in 2008; 'A defense of beanbag genetics').  The author was one John Burdon Sanderson Haldane, better known as JBS Haldane.  Along with RA Fisher and Sewall Wright (and, later Motoo Kimura, James Crow and an expanding array of others) Haldane helped found and then develop the field of population genetics.

See also:

commentary in the reprint issue (including the story behind the first footnote...) from the late James Crow, Haldane and beanbag genetics

PZ Myers, Steve Pinker's hair and the muscles of worms

Update: Parts II and III

[biochemistries]

The idea of genetics as essentially a reductionistic one gene, one trait approach to understanding causation and prediction is still a live one, despite decades of evidence to the contrary... The prevailing paradigm is to collect more data, enumerate more genes and gene variants associated with disease, and other sorts of 'omics' Big Data, and we'll finally understand causation and be able to predict disease. It is largely raw induction--the data will speak for themselves by the patterns computers can find in them. But in many ways, the closer we look, the stranger things seem, not clearer. ... what we get and what most are seeking are just lists, in some ways that only a computer can love (or have the patience to look through), and lists don't account for the many, many spatial and temporal entanglements, of diverse form, between the multitude of factors we know are involved in making organisms what they are, in 4-dimensional space and time. ... Darwin's very Newtonian simple causal determinism was patently imprecise or incomplete. Is there something fundamental about causation in life and genomes that is yet to be discovered?

Ken Weiss asks Do strange things about life require new concepts?

He highlights what is left unsolved in modern Biology, and calls out a lot of the 'paradigms' used as obscuring the fuzzy nature of life... His 18 enigmas are:

The linear view of genetic causation (cis effects of gene function, for the cognoscenti) is clearly inaccurate.  Gene regulation and usage are largely, if not mainly, not just local to a given chromosome region (they are trans);

Chromosomal usage is 4-dimensional within the nucleus, not even 3-dimensional, because arrangements are changing with circumstances, that is, with time;

There is a large amount of inter-genic and inter-chromosomal communication leading to selective expression and non-expression at individual locations and across the genome (e.g., monoallelic expression).  Thousands of local areas of chromosomes wrap and unwrap dynamically depending on species, cell type,  environmental conditions, and the state of other parts of the genome at a given time;

There is all sorts of post-transcription modification (e.g., RNA editing, chaperoning) that is a further part of 4-D causation;

There is environmental feedback in terms of gene usage, some of which is inherited (epigenetic marking) that can be inherited and borders on being 'lamarckian';

There are dynamic symbioses as a fundamental and pervasive rather than just incidental and occasional part of life (e.g., microbes in humans);

There is no such thing as 'the' human genome from which deviations are measured.  Likewise, there is no evolution of 'the' human and chimpanzee genome from 'the' genome of a common ancestor.  Instead, perhaps conceptually like event cones in physics, where the speed of light constrains what has happened or can happen, there are descent cones of genomic variation descending from individual sequences--time-dependent spreading of variation, with time-dependent limitations.  They intertwine among individuals though each individual's is unique.  There is a past cone leading of ancestry to each current instance of a genome sequence, from an ever-widening set of ancestors (as one goes back in time) and a future cone of descendants and their variation that's affected by mutations.  There are descent cones in the genomes among organisms, and among organisms in a species, and between species. This is of course just a heuristic, not an attempt at a literal simile or to steal ideas from physics!

Descent cones exist among the cells and tissues within each organism, because of somatic mutation, but the metaphor breaks down because they have strange singular rather than complex ancestry because in individuals the go back to a point, a single fertilized egg, and of individuals to life's Big Bang;

For the previous reasons, all genomes represent 'point' variations (instances) around a non-existent core  that we conceptually refer to as 'species' or 'organs', etc.('the' human genome, 'the' giraffe, etc.);

Enumerating causation by statistical sampling methods is often impossible (literally) because rare variants don't have enough copies to generate 'significance', significance criteria are subjective, and/or because many variants have effects too small to generate significance;

Natural selection, that generates current variation along with chance (drift) is usually so weak that it cannot be demonstrated, often in principle, for similar statistical reasons:  if cause of a trait is too weak to show, cause of fitness is too weak to show; there is not just one way to be 'adapted'.

Alleles and genotypes have effects that are inherently relativistic.  They depend upon context, and each organism's context is different;

Perhaps analogously with the ideal gas law and its like, phenotypes seem to have coherence.  We each have a height or blood pressure, despite all the variation noted above.  In populations of people, or organs, we find ordinary (e.g., 'bell-shaped') distributions, that may be the result of a 'law' of large numbers: just as human genomes are variation around a 'platonic' core, so blood pressure is the net result of individual action of many cells.  And biological traits are typically always changing;

Genomic-based risks are retrospectively assessed but future environments cannot, in principle, be known, so that genomic-based prediction is an illusion of unclear precision;

The typical picture is of many-to-many genomic (and other) causation for which many causes can lead to the same result (polygenic equivalence), and many results can be due to the same cause (pleiotropy);

We are prisoners of single-cause thinking, which is only reinforced by strongly adaptationist Darwinism that, to this day, makes us think deterministically and in terms of competition, even though life is manifestly a phenomenon of molecularcooperation (interaction).  We have no theory for the form of these interactions (simple multiplicative? geometric?).

In a sense all molecular reactions are about entropy, energy, and interaction among different molecules or whatever.  But while ordinary nonliving molecular reactions converge on some result, life is generally about increasing difference, because life is an evolutionary phenomenon.

DNA is itself a quasi-random, inert sequence. Its properties come entirely from spatial, temporal, combinatorial ('Boolean'-like) relationships. This context works only because of what else is in (and on the immediate outside) of the cell at the given time, a regress back to the origin of life.

Ken Weiss, Are we there yet or do strange things about life require new thinking? Wednesday October 30, 2013