Developmental dynamics and contemporary evolutionary psychology: status quo or irreconcilable views? Reply to Bjorklund (2003), Krebs (2003), Buss and Reeve (2003), Crawford (2003), and Tooby et Al. (2003).
The authors argue that evolutionary psychology currently offers no coherent framework for how to integrate genetic, environmental, and experiential factors into a theory of behavioral or cognitive phenotypes.
We propose a revival of the concept of the ‘Big Bang’ of vertebrate immunity, arguing that its origin involved a ‘difficult’ (i.e. low-probability) evolutionary transition that might have occurred only once, in a common ancestor of all vertebrates. In contrast to the original concept, we argue that the limiting innovation was not the generation of somatic diversity, but the regulatory circuitry needed for the safe operation of amplifiable immune responses with somatically acquired targeting. Regulatory complexity increased abruptly by genomic duplications at the root of the vertebrate lineage, creating a rare opportunity to establish such circuitry. We discuss the selection forces that might have acted at the origin of the transition, and in the subsequent stepwise evolution leading to the modern immune systems of extant vertebrates.
All genomic duplications in vertebrates are food energy-dependent and RNA-mediated. None occur linearly. Natural selection for energy-dependent codon optimality links changes in base pairs to the fixation of amino acid substitutions, which have been linked to all morphological and behavioral diversity by biophysically constrained viral latency.
For example, a single amino acid substitution in the gonadotropin releasing hormone decapeptide links achiral glycine in position 6 to all vertebrate cell type differentiation.
We demonstrate here that a protochordate GnRH receptor does not distinguish GnRHs with achiral or chiral amino acids, whereas GnRH receptors of jawed vertebrates are highly selective for GnRHs with the central achiral glycine. The poor activity of the protochordate GnRH was increased >10-fold at vertebrate receptors by replacement of the chiral amino acid with glycine or a d-amino acid, which favor the type II′ β-turn.
This suggests that amplification of this lncRNA alone (even without MYC) can promote tumorigenesis in breast cancer by increasing MYC expression , which has been proposed to occur by protein stabilization. However, it is unlikely that this is the only mechanism of action for this lncRNA as this multi-exonic transcript encoding over 20 different isoforms is itself under the control of c-MYC and harbours multiple microRNAs within its locus .
Define isoform: any of two or more functionally similar proteins that have a similar but not an identical amino acid sequence.
The fact that a multi-exonic transcript encoding over 20 different proteins with similar but not identical amino acid sequences links the term isoforms from wordplay via multiple food energy-dependent microRNAs and RNA-mediated amino acid substitutions that control the virus-driven degradation of messenger RNA.
…the clear identity and easy alignment of these sequences makes them good candidates for estimating phylogeny, and they can reliably be found and identified across all members of a clade of interest. Their relatively slow evolution  also means that they can easily be identified in de novo assemblies of genomes.
The ridiculous claim about the slow evolution of energy-dependent RNA-mediated amino acid substitutions cannot be put back into any aspect of identification in de novo assemblies of genomes. The assembly of all organized genomes is energy-dependent and biophysically constrained by the pheromone-controlled physiology of reproduction.