Potential falsifications of the theory of evolution

This paper talks of Non-Random Distribution of TEs, where the TEs non-randomly occur in what appears to be selected sites.

However, as mentioned above and observed previously (reviewed in [44]), LINEs, SINEs and some LTR retrotransposon families accumulate preferentially in areas that are near genes.

Overall, LTR retrotransposons are found to be most abundant in pericentromeric heterochromatin and least abundant in the more gene-rich arms on all chromosomes.

Of the 1991 SINEs discovered, 1174 were found in the introns or UTRs (untranslated regions) of genes and 21 in putative coding exons (data not shown).

I was stating that to me the authors of the paper did not state that the TEs were random, but in a sense determstic per shapiro

P element insertion is nonrandom, and most insertions occur within a few hundred bases of the transcription start site of a gene.

It is likely that a great deal of this preference is caused by chromatin accessibility, as these are the same chromosomal regions that must be accessed by the transcriptional control machinery.

In this report we present evidence that this local preference may depend more on DNA structure than on primary sequence.

However wouldn't the number of different TEs that target a location make them more or less determistic, and thus possibly more or less random?

Now if each different TE has a unique effect on the location it targets, then it would be less random to any change in that location.

On average, TEs that insert within the exons of genes are most likely to result in null mutations because of the sensitivity of these regions to frame shift mutations and the lack of tolerance of highly conserved regions to most mutations of any kind. However, those mutations that are not simply inviable can provide interesting and sometimes spectacular phenotypic variability.

Do you accept McCllintocks findings and if so are these random mutations?

He says what were referred to as "random accidents" are regulated biochemical systems that are a source of genetic variation .

Cells don't "learn by trial and error". Nor do they "discover". NGE mechanisms simply respond to various stimuli (stress, etc.) and kick off a biochemical pathway that alters the genome.What we know is that cells have sensory systems and that cells can transmit and process information that these systems generate. The deeper we look into cell sensory and memory systems, such as piRNA loci in animals and CRISPRs in prokaryotes, the more difficult it is to say that any of them are simple. I personally do not know how cell computation works, but I can certainly name a lot of molecules that are involved in those processes. We have a great deal to learn about how cell information-processing operates and influences natural genetic engineering. That, it seems to me, is where our experimental focus should be in evolution science.

95+% of Ty1-4 insertions in Saccharomyces cerevisiae do not insert into exons but upstream of PolIII promoters. They interact with PolIII transcription factors. This is what I mean by non-random. There are many similar biases in NGE, although generally not as strongly biased as Ty elements. Non-random does not mean strictly deterministic, but just about all the systems I know have some kind of targeting interactions. I have tabulated these a number of times (Table 5, Shapiro 2002 Ann NYAS & Table 1, Shapiro 2005, Gene). I recommend you look at these tabulations and the underlying references to get an idea of how extensive this literature is. I also suggest you look at the data on P factor homing to see what highly non-random but also highly non-deterministic targeting can be (e.g. Bender, W. and A. Hudson, P element homing to the Drosophila bithorax complex. Development, 2000. 127(18): p. 3981-92.) Some of these examples will blow your mind and make you think twice before you say "random" again. Let me know if I'm right about that.

P element insertion is essentially random at the scale of the genome.

He is stating that they do this but does not say by trial and error, but by these sensory systems.

The function of a sensory receptor cell is to detect external stimuli and transduce this information into a signal that elicits the appropriate behavioral response. In bacterial chemotaxis stimuli are detected by approximately 20 different types of chemoreceptors which transmit information along a network of converging pathways.

I don't interpret that as being "learn by trial and error."

Maybe you should say "mutations are non-random, but their effect on fitness are not yet known and may well be deterministic".

would you agree that this peer reviewed paper, if correct, describes non-random functions including those of fitness?

What we have in mind is a bacterial version of genome cybernetics, by which we mean the ability of the genome to perform information processing and alter itself accordingly.

The new picture of the genome as an adaptive cybernetic unit with self-awareness is presented in Sections 6-8.

Could, then, our internal and external linguistic communication and social intelligence be traced back to bacteria — the simplest of all organisms?