Change in Genetic Code May Explain How Human Ancestors Lost Tails | NYU Langone News
In that distant, pre-'Creation Week' history of Life On Earth, 25 million years before creationists think Earth was created out of nothing, and all living things on it were magicked into existence without ancestors, a 'jumping gene' inserted a short length of DNA termed AluY, into the gene which controls tail length in monkeys, and the resulting tailless monkeys went on to diversify into the apes - gibbons, siamangs, orangutans, gorillas, chimpanzees, bonobos, and the hominins which were to evolve into the Australopithecines and the Homo genus, including Homo sapiens, all of which still possess that short insertion in the TBXT gene, which otherwise is identical to one of the gene which grow the tail of the simians.
As an example of design, it is one of the least intelligent, since, instead of removing all the genes required to grow a tail, the 'designer' simply broke an essential gene and left all the others to do nothing apart from having to be replicated in every cell in every ape that ever lived, as an example of the massive waste and unnecessary complexity that characterises an evolved process and gives the lie to any notion of any intelligence being involved.
By inserting the AluY snippet into a mouse BBXT gene the researchers found a variety of tail effects, including mice born without tails. They also showed that there was a small increase in the incidence on neural tube defects (spina bifida) in mice.
Quite why tailless would have been selected for during the evolution of these ancestors of the modern apes is a matter for speculation; maybe a tail was becoming an encumbrance for a brachiating mode of locomotion as opposed to running along the top of branches and jumping from branch to branch, which the smaller monkeys used, where a tail was an important balance organ. For a heavier ape hanging beneath the branches by its arms, there would have been less need for a balance organ and a tail would have been liable to damage and infection.
How this was discovered by a team led by researchers at New York University Grossman School of Medicine, is the subject of an open access paper in Nature and a NYU Langone Health news release:
A genetic change in our ancient ancestors may partly explain why humans don’t have tails like monkeys, finds a new study led by researchers at NYU Grossman School of Medicine.
Published online February 28 as the cover story of the journal Nature, the work compared the DNA of tailless apes and humans to that of tailed monkeys. It found an insertion of DNA shared by apes and humans but missing in monkeys. When the research team engineered a series of mice to examine whether the insertion, in a gene called TBXT, affected their tails, they found a variety of tail effects, including some mice born without tails.
“Our study begins to explain how evolution removed our tails, a question that has intrigued me since I was young,” says lead study author Bo Xia, PhD, a graduate student at the time of the study in the labs of study senior co-authors Jef D. Boeke, PhD, and Itai Yanai, PhD , at NYU Grossman School of Medicine. Dr. Xia is now a junior fellow of the Harvard Society of Fellows and a principal investigator at the Broad Institute of MIT and Harvard.
More than 100 genes had been linked by past work to the development of tails in various vertebrate species, and the study authors hypothesized that tail loss occurred through changes in the DNA code (mutations) of one or more of them. Remarkably, say the study authors, the new study found that the differences in tails came not from TBXT mutations but instead from the insertion of a DNA snippet called AluY into the gene’s regulatory code in the ancestors of apes and humans.
Profound Surprise
The new finding proceeds from the process by which genetic instructions are converted into proteins, the molecules that make up the body’s structures and signals. DNA is “read” and converted into a related material in RNA, and ultimately into mature messenger RNA (mRNA), which produces proteins.
In a key step that produces mRNA, “spacer” sections called introns are cut out of the code, but before this happens they guide the stitching together (splicing) of just the DNA sections, called exons, that encode the final instructions. Further, the genomes of vertebrate animals evolved to feature alternative splicing, in which a single gene can code for more than one protein by leaving out or adding exon sequences. Beyond splicing, the human genome grew more complex still by evolving to include “countless” switches, part of the poorly understood “dark matter” that turns on genes at different levels in different cell types.
Still other work has shown that half of this non-gene “dark matter” in the human genome, which lies both between genes and within the introns, consists of highly repeated DNA sequences. In addition, most of these repeats consist of retrotransposons, also called “jumping genes” or “mobile elements,” which can move around and insert themselves repeatedly and randomly in human code.
Pulling these details together, the “astounding” current study found that the transposon insertion of interest, AluY, which affected tail length, had randomly occurred in an intron within the TBXT code. Although it did not change a coding portion, the intron insertion, the research team showed, influenced alternative splicing, something not seen before, to result in a variety of tail lengths. Dr. Xia found an AluY insertion that remained in the same location within the TBXT gene in humans and apes resulted in the production of two forms of TBXT RNA. One of these, the researchers theorize, directly contributed to tail loss.
Tail loss in the group of primates that includes gorillas, chimpanzees, and humans is believed to have occurred about 25 million years ago, when the group evolved away from Old World monkeys, said the authors. Following this evolutionary split, the group of apes that includes present-day humans evolved the formation of fewer tail vertebrae, giving rise to the coccyx, or tailbone. Although the reason for tail loss is uncertain, some experts propose that it may have better suited life on the ground than in the trees.This finding is remarkable, because most human introns carry copies of repetitive, jumping DNAs without any effect on gene expression, but this particular AluY insertion did something as obvious as determine tail length.
Professor Dr. Jef D. Boeke, corresponding author
Sol and Judith Bergstein Director of the Institute for Systems Genetics
Department of Biochemistry and Molecular Pharmacology
Institute for Systems Genetics
NYU Langone Health, New York, NY, USA
Any advantage that came with tail loss was likely powerful, the researchers say, because it may have happened despite coming with a cost. Genes often influence more than one function in the body, so changes that bring an advantage in one place may be detrimental elsewhere. Specifically, the research team found a small uptick in neural tube defects in mice with the study insertion in the TBXT gene.
Future experiments will test the theory that in an ancient evolutionary trade-off, the loss of a tail in humans contributed to the neural tube birth defects, like those involved in spinal bifida, that are seen today in one in a thousand human neonates.
Professor Dr. Itai Yanai, co-corresponding author
Director of the Institute for Computational Medicine. Institute for Systems Genetics
NYU Langone Health, New York, NY, USA
AbstractWhat creationists need to decide now is whether this mutation was an evolutionary change, given their superstition that humans are the supreme creation, or whether it was 'devolutionary' like Michael J Behe says all mutations are.
The loss of the tail is among the most notable anatomical changes to have occurred along the evolutionary lineage leading to humans and to the ‘anthropomorphous apes’1,2,3, with a proposed role in contributing to human bipedalism4,5,6. Yet, the genetic mechanism that facilitated tail-loss evolution in hominoids remains unknown. Here we present evidence that an individual insertion of an Alu element in the genome of the hominoid ancestor may have contributed to tail-loss evolution. We demonstrate that this Alu element—inserted into an intron of the TBXT gene7,8,9—pairs with a neighbouring ancestral Alu element encoded in the reverse genomic orientation and leads to a hominoid-specific alternative splicing event. To study the effect of this splicing event, we generated multiple mouse models that express both full-length and exon-skipped isoforms of Tbxt, mimicking the expression pattern of its hominoid orthologue TBXT. Mice expressing both Tbxt isoforms exhibit a complete absence of the tail or a shortened tail depending on the relative abundance of Tbxt isoforms expressed at the embryonic tail bud. These results support the notion that the exon-skipped transcript is sufficient to induce a tail-loss phenotype. Moreover, mice expressing the exon-skipped Tbxt isoform develop neural tube defects, a condition that affects approximately 1 in 1,000 neonates in humans10. Thus, tail-loss evolution may have been associated with an adaptive cost of the potential for neural tube defects, which continue to affect human health today.
Main
The tail appendage varies widely in its morphology and function across vertebrate species4,6. For primates in particular, the tail is adapted to a range of environments, with implications for the style of locomotion of the animal11,12. The New World howler monkeys, for example, evolved a prehensile tail that helps with the grasping or holding of objects while occupying arboreal habitats13. Hominoids—which include humans and the apes—however, lost their external tail during evolution. The loss of the tail is inferred to have occurred around 25 million years ago when the hominoid lineage diverged from the ancient Old World monkeys (Fig. 1a), leaving only 3–5 caudal vertebrae to form the coccyx, or tailbone, in modern humans14.It has long been speculated that tail loss in hominoids contributed to orthograde and bipedal locomotion, the evolutionary occurrence of which coincided with the loss of the tail15,16,17. Yet, the genetic mechanism that facilitated either tail-loss evolution or orthograde and bipedal locomotion in hominoids remains unknown. Recent progress in primate genome sequencing projects have made it possible to infer causal links between genotypic and phenotypic changes18,19,20, and have enabled the search for hominoid-specific genetic elements that control tail development21. Moreover, developmental genetics studies of vertebrates have led to the elucidation of the gene regulatory networks that underlie tail development21,22. For example, the Mouse Genome Informatics (MGI) database includes more than 100 genes identified from natural mutants and induced mutagenesis studies relating to the absence or shortening of the tail phenotype22,23 (Supplementary Data 1 and Methods). Expression of these genes, including the core factors for inducing mesoderm and definitive endoderm such as Tbxt (also called T or Brachyury), Wnt3a and Msgn1, is enriched in the development of the primitive streak and posterior body formation. Although perturbations of these genes may lead to the shortening or complete absence of the tail, the causal genetic changes that drove the evolution of tail-loss in hominoids remains unknown. Understanding the genetics of tail loss in hominoids may provide insight into the evolutionary pressure that led to human traits such as bipedalism.Fig. 1: Evolution of tail loss in hominoids.
a, Tail phenotypes across the primate phylogenetic tree. Ma, millions of years ago. b, UCSC Genome browser view51 of the conservation score through multi-species alignment at the TBXT locus across primate genomes. Exon numbering of human TBXT follows a conventional order across species without including the 5′ untranslated region exon. The hominoid-specific AluY element is highlighted in red. LINE, long interspersed nuclear element; LTR, long terminal repeat; SINE, short interspersed nuclear element. c, Schematic of the proposed mechanism of tail-loss evolution in hominoids. Primate images in a and c were created using BioRender (https://biorender.com).Fig. 3: The TBXTΔexon6 isoform is sufficient to induce tail-loss phenotype.
a, CRISPR design for generating the TbxtΔexon6/+ heterozygous mouse model. b, Schematic of TBXT transcripts in human and mouse models. TbxtΔexon6/+ mouse mimics TBXT gene expression products in humans. c, Sanger sequencing of the RT–PCR product confirmed that deleting exon 6 in mouse Tbxt leads to correct splicing by fusing exons 5 and 7. d, A representative TbxtΔexon6/+ founder mouse (day 1) exhibiting a no-tail phenotype. Two additional founder mice are shown in Extended Data Fig. 5. e, TbxtΔexon6/+ mice exhibit heterogeneous tail phenotypes, varying from no tail to long tails. cv, caudal vertebrae; sv, sacral vertebrae; WT, wild type; arrowheads highlight differences in tail phenotypes.
Then there are the small matters of why this mutation is present in all the other apes and why an intelligent designer would give us and the other apes the genes for making a tail, then just break one of them so the tail doesn't develop and the fact that this all happened 25 million years before 'Creation Week'.
And lastly, there is the evidence that this 'design' increases the risk of spina bifida - which any omniscient designer should have been aware of. On the principle that whatever an omniscient designer's designs do, is what they were designed to do, creationists need to explain why their putative designer god intended children to be born with a serious birth defect.
But small problems that are utterly irreconcilable with a belief in a 6-day creation, 10,000 years ago by an intelligent, omnibenevolent designer, are not normally regarded as a problem for creationism.
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