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| Humans and fish share about 70% of their protein-coding genes, but only about 0.5% of their regulatory long noncoding RNAs (lncRNAs) |
And another sacred creationist dogma crashes and burns.
Imagine! You're a creationist fraud trying to make an even better living by taking yet more money off people who feel so important that they believe they must have a close personal relationship with the creator of the Universe! You're feeding them all sorts of sciencey-sounding stuff because, despite convincing them that science is all wrong, they still have a nagging doubt that it might not be, so, to be on the safe side, you want them to think that even if it is right occasionally, it supports their preconceived ideas and confirms that they know better than all those wacky scientists.
You've convinced them that something called the Second Law, combined with something really mysterious that only really clever people can understand called Information Theory means that evolution can't happen, because it would mean creating new information - and that is impossible. You've sold them the idea that mutations are always harmful so any mutation in DNA would result in virtually instant death with no hope of passing it on and anyway, even it it was passed on, the offspring wouldn't survive.
You've even got them using computers and swarming the Internet telling bemused scientists and other educated people that they've got everything all wrong and science has failed, without the least sense of irony!
Then along come a team of scientists and publish a scientific paper in a peer-reviewed scientific journal, complete with evidence and pictures and long words, that explains how we got a lot of our genes through mutations of old ones and that mutations have given them completely new information, so now they have a different function to the originals in creatures in our remote ancestry a couple of hundred million of years ago.
The question now is how do you misrepresent the science? Do you ignore it altogether? Do you lie about it? Do you dismiss it all as a big conspiracy? Or do you just do what others do and declare that anything you and they disagree with must be wrong, by definition?
That's the dilemma now facing the Hams, Hovinds, Behes and Demskys of the creation industry. They're not going to accept the evidence, admit they were wrong and go and look for proper jobs of course. The money is too good and the living is too easy.
In fact, the science shows is that not only are there as many as 20,000 long non-coding RNA (lncRNA) genes in the human genome – about the same number as the protein-coding ones – but the lncRNAs have lately been revealed to serve as master switches in a wide variety of biological processes. They turn genes on and off and affect other regulatory genes, controlling cellular fate during fetal development, as well as cellular division and death in the adult organism. These master regulators may therefore hold the key to elucidating or even treating a variety of diseases.
Igor Ulitsky and his team – research students Hadas Hezroni, Gali Housman and Zohar Meir, and staff scientists Drs. Rotem Ben-Tov Perry and Yoav Lubelsky of the Weizmann Institute of Science - managed to identify a class of mammalian lncRNAs that had evolved from more ancient genes by taking on new functions.
His team members developed a series of algorithms that enabled them to find such “recycled” genes in the mammalian genome. First, they identified nearly 1,000 genes that code for proteins in chickens, fish, lizards and other non-mammalian vertebrates, but not in humans, dogs, sheep and other mammals. The scientists hypothesized that at least some of these genes, after losing their protein-coding function, started manufacturing lncRNAs in mammals. By comparing “gene neighborhoods” in the vicinity of lncRNAs and of genes that had stopped coding for proteins, the researchers revealed that indeed, about 60 lncRNA genes in mammals – or 2% to 3% of lncRNAs shared by humans and other mammalian species – appear to be derived from ancestral genes. Their genetic sequence is in some cases similar to that of the ancient genes, but they have lost their protein-coding ability.
“It is hard to know what caused these genes to lose their protein-coding potential more than 200 million years ago, when mammals evolved from their vertebrate ancestors,” Ulitsky says. “But the fact that these genes have been conserved in the genome for so long suggests that they play important roles in the cell.”
Identifying such “fossils” of protein-coding genes in the mammalian genome will facilitate further study of human lncRNAs and may ultimately help scientists understand what happens when their function is disrupted. For example, lncRNAs help create different types of neurons in the fetal brain; their failure to properly determine the fate of these neurons may contribute to epilepsy. Because lncRNAs are involved in controlling cell division, their malfunction may be implicated in cancer. Finally, manipulating lncRNAs may make it possible to treat certain genetic disorders.
As the scientists say in an open access paper in Genome Biology:
Abstract
Background
Only a small portion of human long non-coding RNAs (lncRNAs) appear to be conserved outside of mammals, but the events underlying the birth of new lncRNAs in mammals remain largely unknown. One potential source is remnants of protein-coding genes that transitioned into lncRNAs.
Results
We systematically compare lncRNA and protein-coding loci across vertebrates, and estimate that up to 5% of conserved mammalian lncRNAs are derived from lost protein-coding genes. These lncRNAs have specific characteristics, such as broader expression domains, that set them apart from other lncRNAs. Fourteen lncRNAs have sequence similarity with the loci of the contemporary homologs of the lost protein-coding genes. We propose that selection acting on enhancer sequences is mostly responsible for retention of these regions. As an example of an RNA element from a protein-coding ancestor that was retained in the lncRNA, we describe in detail a short translated ORF in the JPX lncRNA that was derived from an upstream ORF in a protein-coding gene and retains some of its functionality.
Conclusions
We estimate that ~ 55 annotated conserved human lncRNAs are derived from parts of ancestral protein-coding genes, and loss of coding potential is thus a non-negligible source of new lncRNAs. Some lncRNAs inherited regulatory elements influencing transcription and translation from their protein-coding ancestors and those elements can influence the expression breadth and functionality of these lncRNAs.
Hadas Hezroni, Rotem Ben-Tov Perry, Zohar Meir, Gali Housman, Yoav Lubelsky and Igor Ulitsky
A subset of conserved mammalian long non-coding RNAs are fossils of ancestral protein-coding genes
Genome Biology201718:162 https://doi.org/10.1186/s13059-017-1293-0
© 2017 The Authors.
Published open access
Reprinted under the terms of the Creative Commons Attribution 4.0 International License (CC BY 4.0)
So, about 55 'fossil' protein-coding genes in the human genome from 200 million years ago have not only mutated without harming their hosts but they have evolved new processes and been co-opted for entirely new uses by radically changing the information they contain.
How's that for impossible?
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