Brochosome Proteins Encoded By Orphan Genes

As to this claim: “It is possible that secreta exported from the organism may evolve especially rapidly because they are not strongly constrained by interactions with other traits.”

"And how did all these orphan genes arise so rapidly? The paper hypothesizes that “It is possible that secreta exported from the organism may evolve especially rapidly because they are not strongly constrained by interactions with other traits.” That evolutionists can so easily reach for just-so stories, such as this, is yet another example of how false predictions have no consequence for evolutionary theory.,,,"

That claim is falsified by the fact that many orphans are now found to play essential roles,,,

"Next evolutionists thought that these rapidly-evolving unique genes must not code for functional or important proteins. But again, many of the unique proteins were in fact found to play essential roles. (Chen, Zhang and Long 1010; Daubin and Ochman; Pilcher) As one researcher explained, “This goes against the textbooks, which say the genes encoding essential functions were created in ancient times.” (Pilcher)" - Cornelius Hunter https://sites.google.com/site/darwinspredictions/similar-species-share-similar-genes

As alluded to above, and completely contrary to evolutionary thought, these 'new' ORFan genes are found to be just as essential as 'old' genes for maintaining life:

Age doesn't matter: New genes are as essential as ancient ones - December 2010 Excerpt: "A new gene is as essential as any other gene; the importance of a gene is independent of its age," said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. "New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked." http://www.sciencedaily.com/releases/2010/12/101216142523.htm New genes in Drosophila quickly become essential. - December 2010 Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages. http://www.sciencemag.org/content/330/6011/1682.abstract Can new genes arise from junk DNA? - August 2015 Excerpt: Researchers are beginning to understand that de novo genes seem to make up a significant part of the genome, yet scientists have little idea of how many there are or what they do. What’s more, mutations in these genes can trigger catastrophic failures. “It seems like these novel genes are often the most important ones,” said Erich Bornberg-Bauer, a bioinformatician at the University of Münster in Germany.,,, Scientists also want to understand how de novo genes get incorporated into the complex network of reactions that drive the cell, a particularly puzzling problem. It’s as if a bicycle spontaneously grew a new part and rapidly incorporated it into its machinery, even though the bike was working fine without it. “The question is fascinating but completely unknown,” Begun said. A human-specific gene called ESRG illustrates this mystery particularly well. Some of the sequence is found in monkeys and other primates. But it is only active in humans, where it is essential for maintaining the earliest embryonic stem cells. And yet monkeys and chimps are perfectly good at making embryonic stem cells without it. “It’s a human-specific gene performing a function that must predate the gene, because other organisms have these stem cells as well,” McLysaght said. “How does novel gene become functional? How does it get incorporated into actual cellular processes?” McLysaght said. “To me, that’s the most important question at the moment.” https://www.quantamagazine.org/20150818-a-surprise-source-of-lifes-code/

Moreover, besides Orphan genes, "Alternative splicing can produce variant proteins and expression patterns as different as the products of different genes."

Frequent Alternative Splicing of Human Genes – 1999 Excerpt: Alternative splicing can produce variant proteins and expression patterns as different as the products of different genes. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC310997/

On top of that "the total number of proteins in human cells, produced by the approx. 20,000 genes is estimated to be (via alternative splicing) between 250,000 to one million."

What is Cancer Proteomics? Excerpt: One gene can encode more than one protein (even up to 1,000). The human genome contains about 21,000 protein-encoding genes, but the total number of proteins in human cells is estimated to be (via alternative splicing) between 250,000 to one million. https://proteomics.cancer.gov/whatisproteomics Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing - 2016 In Brief Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,, Page 806 excerpt: As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms (Smith and Kelleher, 2013). http://iakouchevalab.ucsd.edu/publications/Yang_Cell_OMIM_2016.pdf

Moreover, "alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,”"

Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012 Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,, A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species. On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,, http://www.the-scientist.com/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%2F

Simply put, Alternative splicing, (one gene coding for multiple different proteins), patterns (that vary widely between even supposedly closely related species), blows Darwinian assumptions out of the water:

Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - published online May 2013 Excerpt: In the last decade, we have discovered still another aspect of the multi- dimensional genome. We now know that DNA sequences are typically “ poly-functional”,,, According to Kapronov et al., “it is not unusual that a single base-pair can be part of an intricate network of multiple isoforms of overlapping sense and antisense transcripts, the majority of which are unannotated” [41]. The ENCODE project [42] has confirmed that this phenomenon is ubiquitous in higher genomes, wherein a given DNA sequence routinely encodes multiple overlapping messages, meaning that a single nucleotide can contribute to two or more genetic codes. Most recently, Itzkovitz et al. analyzed protein coding regions of 700 species, and showed that virtually all forms of life have extensive overlapping information in their genomes [43]. Conclusions: Our analysis confirms mathematically what would seem intuitively obvious - multiple overlapping codes within the genome must radically change our expectations regarding the rate of beneficial mutations. As the number of overlapping codes increases, the rate of potential beneficial mutation decreases exponentially, quickly approaching zero. http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006

bornagain77

April 9, 2018

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