WORLDNET ARCHIVES ADVISORY: the following is an excerpt from the discussion section of a scientific research article written in a dry, complex style with technical terms.
Title: “Evolutionary human genomic extrapolations: pseudogene-to-gene emergence within human chromosome nine.”
Author: Ian M. Gardiner; Institute of Structural and Molecular Biology, Birkbeck, University of London, London, (formerly) U.K.
Source: Journal of Theoretical Genomics, vol. 6, no. 2, pp 23-46.
Date of original peer-reviewed epublication: 03/02/2040 (pre-WorldNet internet).
Date of WorldNet upload: 05/23/2048.
[Beginning of excerpt] (…) The mutational simulations and probabilities of allelic penetrance I provided in this paper, and which incorporate natural rates of mutation, indicate the likelihood of the emergence of two recessive, yet complementary, alleles carried by human chromosome 9.
The first hypothetical allele, designated as the A (‘Actualizing’)-allele, lies within the HChr9p11.2 region and, specifically, at location HChr9: 40,755,407-40,767,875.
A single base pair insertion in this site results in a gene promoter-type DNA-binding sequence recognized by either the estradiol-responsive or testosterone-responsive transcription factors. Furthermore, this same base pair insertion shifts the downstream reading frame of the pseudogene contiguous to the newly formed promoter, thus giving rise to a novel functional gene. Hence, this ‘new’ gene would be one actuated at the onset of puberty, resulting in the expression of a novel and unique transcription factor which I hereby designate as AFAE-1 (‘Actualizing Factor, Aptitude-Enhanced-1’).
In contrast to the A-allele, the second hypothetical, designated E (‘Effector’)-allele comprises a sizeable portion of human chromosome 9 (HChr9q12/13→9q22.32 region; specific HChr9 location range: 60,546,920-97,700,734), one noted to be non-coding or pseudogene-rich and virtually void of functional genes.
My multivarious mutational simulations in this region of HChr9 reveal potential clusters of pseudogenes with potential to become functional genes, all of which wind up falling under the primary control of AFAE-1 for their activation and expression. Incidentally, these distinct ‘new’ gene clusters are expressed under tissue-specific contexts such as the brain, the skeletal muscles, or the skin. Moreover, I identified between two and three sub-clusters per each tissue-specific cluster, thus opening the possibility of further distinctions in functionalities. However, only one tissue-specific gene sub-cluster may emerge at a time; nonetheless, this suggests variability (albeit somewhat limited) for this putative E-allele.
At the present time, it remains out of scope for this paper to assign physiological functions to each possible tissue-specific gene sub-cluster I identified. Nevertheless, in the advent of the emergence of any one of such E-allele sub-clusters, and because these depend first and foremost on AFAE-1 for their activation, I therefore expect the expression of tissue-specific, physiological/functional enhancements exclusively in those human individuals carrying both the A and E alleles.
This brings up the second part of this paper, whereby I established multi-factorial and multi-variance probabilistic assessments (or extrapolations) of the temporal emergence and penetrance of these two potential, recessive alleles within the present-day global human gene pool.
I acknowledge the extrapolations provided here cannot account for possible impacts from genetic drift, especially when considering the plethora of regional and global variables used in the calculations of said extrapolations. Indeed, many such variables are subjected to unpredictable modifications, or even nullification, caused by short- or long-term disruptive events (e.g. market downturns/crashes, epidemics/pandemics, minor/major military conflicts, etc.).
Notwithstanding, my calculated genomic extrapolations suggest the A- and E-alleles already penetrated the human population gene pool with rather significant, predicted numbers of heterozygous A/– or E/– carriers worldwide. It is equally noteworthy these same calculations furthermore unveil the definite likelihood of ‘aptitude-enhanced’ A/E heterozygous individuals walking among us presently.
This, in turn, raises the germane questions of whether such men and women do verily live in our societies and, if so, why are they yet to reveal themselves (…) [End of excerpt].
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