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Artificial Selection
3 weeks ago
General
This is a work of fiction. Names, characters, businesses, places, events and incidents are either the products of the author’s imagination or used in a fictitious manner. Any resemblance to actual persons, living or dead, or actual events is purely coincidental.
Artificial selection is inherently destructive, as artificial selection takes away the most fit to reproduce from the gene pool. Natural selection, on the other hand, is naturally constructive and not only builds a stronger genetic code, but reinforces its strength over deep time. Genetic pollution caused by hunting is much more serious in scope than carbon dioxide, arguably comparable to the commercial genetic modification of plants.
Elephants have evolved to be tuskless because of ivory poaching, a study finds
https://www.npr.org/2021/10/22/1048.....oaching-africa
WASHINGTON — A hefty set of tusks is usually an advantage for elephants, allowing them to dig for water, strip bark for food and joust with other elephants. But during episodes of intense ivory poaching, those big incisors become a liability.
Now researchers have pinpointed how years of civil war and poaching in Mozambique have led to a greater proportion of elephants that will never develop tusks.
During the conflict from 1977 to 1992, fighters on both sides slaughtered elephants for ivory to finance war efforts. In the region that's now Gorongosa National Park, around 90% of the elephants were killed.
The survivors were likely to share a key characteristic: half the females were naturally tuskless — they simply never developed tusks — while before the war, less than a fifth lacked tusks.
Like eye color in humans, genes are responsible for whether elephants inherit tusks from their parents. Although tusklessness was once rare in African savannah elephants, it's become more common — like a rare eye color becoming widespread.
After the war, those tuskless surviving females passed on their genes with expected, as well as surprising, results. About half their daughters were tuskless. More perplexing, two-thirds of their offspring were female.
The years of unrest "changed the trajectory of evolution in that population," said evolutionary biologist Shane Campbell-Staton, based at Princeton University.
With colleagues, he set out to understand how the pressure of the ivory trade had tipped the scale of natural selection. Their findings were published Thursday in the journal Science.
Evolutionary changes aren't necessarily slow
Their genetic analysis revealed two key parts of the elephants' DNA that they think play a role in passing on the trait of tusklessness. The same genes are associated with the development of teeth in other mammals.
"They've produced the smoking-gun evidence for genetic changes," said Chris Darimont, a conservation scientist at the University of Victoria in Canada, who was not involved in the research. The work "helps scientists and the public understand how our society can have a major influence on the evolution of other life forms."
Most people think of evolution as something that proceeds slowly, but humans can hit the accelerator.
"When we think about natural selection, we think about it happening over hundreds, or thousands, of years," said Samuel Wasser, a conservation biologist at the University of Washington, who was not involved in the research. "The fact that this dramatic selection for tusklessness happened over 15 years is one of the most astonishing findings."
Now the scientists are studying what more tuskless elephants means for the species and its savannah environment. Their preliminary analysis of fecal samples suggests the Gorongosa elephants are shifting their diet, without long incisors to peel bark from trees.
"The tuskless females ate mostly grass, whereas the tusked animals ate more legumes and tough woody plants," said Robert Pringle, a co-author and biologist at Princeton University. "These changes will last for at least multiple elephant generations."
History of Chronic Wasting Disease
https://wildlife.tamu.edu/cwdhistory/
Origins
The precise location and mode of CWD development is not known. The condition was first noted in 1967 in research mule deer herds in Colorado, but not confirmed as a TSE until the 1970s. By the late 1970s, CWD was recognized in captive facilities in Colorado and Wyoming in mule deer, black-tailed deer, and elk. In 1981, the disease was identified first in the wild in elk in Colorado, followed shortly by mule deer in 1985 in both Colorado and Wyoming. At that time, an endemic zone for the disease was established in those states. CWD, however, spread to captive herds in Saskatchewan, Canada in the mid-1990s, and to Oklahoma and Nebraska, and wild cervids in Saskatchewan by the year 2000.
It was not until 2001 that CWD was identified in white-tailed deer, in South Dakota wild herds, and in a captive herd in Nebraska. In the following years, CWD spread to Minnesota, Wisconsin, New Mexico, Utah, Illinois, Kansas, Virginia, North Dakota, Iowa, Pennsylvania, Texas in 2012, and finally Ohio in 2014. In 2015, Michigan confirmed the first case of CWD in wild white-tailed deer. Currently 21 states and 2 Canadian provinces have CWD.
While CWD was first detected in captive mule deer, it has long-since spread to other cervids. Early reports indicated that transmission outside of mule deer was not possible, followed shortly by infection detected in elk. Eventually, infections in white-tailed deer, moose, and black-tailed deer (sub-species of mule deer) were detected. More recently, red deer were determined susceptible to infection in a research facility.
Chronic wasting disease: change in documented distribution in North America 2000-2024
https://www.usgs.gov/media/images/c.....rica-2000-2024
The role of genetics in chronic wasting disease of North American cervids
https://pmc.ncbi.nlm.nih.gov/articles/PMC7082092/
Abstract
Chronic wasting disease (CWD) is a major concern for the management of North American cervid populations. This fatal prion disease has led to declines in populations which have high CWD prevalence and areas with both high and low infection rates have experienced economic losses in wildlife recreation and fears of potential spill-over into livestock or humans. Research from human and veterinary medicine has established that the prion protein gene (Prnp) encodes the protein responsible for transmissible spongiform encephalopathies (TSEs). Polymorphisms in the Prnp gene can lead to different prion forms that moderate individual susceptibility to and progression of TSE infection. Prnp genes have been sequenced in a number of cervid species including those currently infected by CWD (elk, mule deer, white-tailed deer, moose) and those for which susceptibility is not yet determined (caribou, fallow deer, sika deer). Over thousands of sequences examined, the Prnp gene is remarkably conserved within the family Cervidae; only 16 amino acid polymorphisms have been reported within the 256 amino acid open reading frame in the third exon of the Prnp gene. Some of these polymorphisms have been associated with lower rates of CWD infection and slower progression of clinical CWD. Here we review the body of research on Prnp genetics of North American cervids. Specifically, we focus on known polymorphisms in the Prnp gene, observed genotypic differences in CWD infection rates and clinical progression, mechanisms for genetic TSE resistance related to both the cervid host and the prion agent and potential for natural selection for CWD-resistance. We also identify gaps in our knowledge that require future research.
Survival and selection
The survival advantage conferred by decreased CWD susceptibility can be sufficient to alter population dynamics and provide selective pressure favoring disease resistance (demonstrated for the 96S allele in white-tailed deer, in press20). Such selective pressure is rarely measurable in wild populations, and indicates the potential for CWD to impact cervid populations. Additional genetic work will be needed to evaluate potential selective pressure on other loci and in other species to understand future trends in CWD epidemics and deer populations. Further, we currently lack information about non-disease related fitness characteristics associated with Prnp genetics. This is fertile ground for future selection studies. Future research such as simulation modeling might be used to address questions of how selective pressure could change as disease prevalence alters infection hazard, as agent strains shift, or how animal movement affects disease dynamics in wildlife populations.
Elephants have evolved to be tuskless because of ivory poaching, a study finds
https://www.npr.org/2021/10/22/1048.....oaching-africa
WASHINGTON — A hefty set of tusks is usually an advantage for elephants, allowing them to dig for water, strip bark for food and joust with other elephants. But during episodes of intense ivory poaching, those big incisors become a liability.
Now researchers have pinpointed how years of civil war and poaching in Mozambique have led to a greater proportion of elephants that will never develop tusks.
During the conflict from 1977 to 1992, fighters on both sides slaughtered elephants for ivory to finance war efforts. In the region that's now Gorongosa National Park, around 90% of the elephants were killed.
The survivors were likely to share a key characteristic: half the females were naturally tuskless — they simply never developed tusks — while before the war, less than a fifth lacked tusks.
Like eye color in humans, genes are responsible for whether elephants inherit tusks from their parents. Although tusklessness was once rare in African savannah elephants, it's become more common — like a rare eye color becoming widespread.
After the war, those tuskless surviving females passed on their genes with expected, as well as surprising, results. About half their daughters were tuskless. More perplexing, two-thirds of their offspring were female.
The years of unrest "changed the trajectory of evolution in that population," said evolutionary biologist Shane Campbell-Staton, based at Princeton University.
With colleagues, he set out to understand how the pressure of the ivory trade had tipped the scale of natural selection. Their findings were published Thursday in the journal Science.
Evolutionary changes aren't necessarily slow
Their genetic analysis revealed two key parts of the elephants' DNA that they think play a role in passing on the trait of tusklessness. The same genes are associated with the development of teeth in other mammals.
"They've produced the smoking-gun evidence for genetic changes," said Chris Darimont, a conservation scientist at the University of Victoria in Canada, who was not involved in the research. The work "helps scientists and the public understand how our society can have a major influence on the evolution of other life forms."
Most people think of evolution as something that proceeds slowly, but humans can hit the accelerator.
"When we think about natural selection, we think about it happening over hundreds, or thousands, of years," said Samuel Wasser, a conservation biologist at the University of Washington, who was not involved in the research. "The fact that this dramatic selection for tusklessness happened over 15 years is one of the most astonishing findings."
Now the scientists are studying what more tuskless elephants means for the species and its savannah environment. Their preliminary analysis of fecal samples suggests the Gorongosa elephants are shifting their diet, without long incisors to peel bark from trees.
"The tuskless females ate mostly grass, whereas the tusked animals ate more legumes and tough woody plants," said Robert Pringle, a co-author and biologist at Princeton University. "These changes will last for at least multiple elephant generations."
History of Chronic Wasting Disease
https://wildlife.tamu.edu/cwdhistory/
Origins
The precise location and mode of CWD development is not known. The condition was first noted in 1967 in research mule deer herds in Colorado, but not confirmed as a TSE until the 1970s. By the late 1970s, CWD was recognized in captive facilities in Colorado and Wyoming in mule deer, black-tailed deer, and elk. In 1981, the disease was identified first in the wild in elk in Colorado, followed shortly by mule deer in 1985 in both Colorado and Wyoming. At that time, an endemic zone for the disease was established in those states. CWD, however, spread to captive herds in Saskatchewan, Canada in the mid-1990s, and to Oklahoma and Nebraska, and wild cervids in Saskatchewan by the year 2000.
It was not until 2001 that CWD was identified in white-tailed deer, in South Dakota wild herds, and in a captive herd in Nebraska. In the following years, CWD spread to Minnesota, Wisconsin, New Mexico, Utah, Illinois, Kansas, Virginia, North Dakota, Iowa, Pennsylvania, Texas in 2012, and finally Ohio in 2014. In 2015, Michigan confirmed the first case of CWD in wild white-tailed deer. Currently 21 states and 2 Canadian provinces have CWD.
While CWD was first detected in captive mule deer, it has long-since spread to other cervids. Early reports indicated that transmission outside of mule deer was not possible, followed shortly by infection detected in elk. Eventually, infections in white-tailed deer, moose, and black-tailed deer (sub-species of mule deer) were detected. More recently, red deer were determined susceptible to infection in a research facility.
Chronic wasting disease: change in documented distribution in North America 2000-2024
https://www.usgs.gov/media/images/c.....rica-2000-2024
The role of genetics in chronic wasting disease of North American cervids
https://pmc.ncbi.nlm.nih.gov/articles/PMC7082092/
Abstract
Chronic wasting disease (CWD) is a major concern for the management of North American cervid populations. This fatal prion disease has led to declines in populations which have high CWD prevalence and areas with both high and low infection rates have experienced economic losses in wildlife recreation and fears of potential spill-over into livestock or humans. Research from human and veterinary medicine has established that the prion protein gene (Prnp) encodes the protein responsible for transmissible spongiform encephalopathies (TSEs). Polymorphisms in the Prnp gene can lead to different prion forms that moderate individual susceptibility to and progression of TSE infection. Prnp genes have been sequenced in a number of cervid species including those currently infected by CWD (elk, mule deer, white-tailed deer, moose) and those for which susceptibility is not yet determined (caribou, fallow deer, sika deer). Over thousands of sequences examined, the Prnp gene is remarkably conserved within the family Cervidae; only 16 amino acid polymorphisms have been reported within the 256 amino acid open reading frame in the third exon of the Prnp gene. Some of these polymorphisms have been associated with lower rates of CWD infection and slower progression of clinical CWD. Here we review the body of research on Prnp genetics of North American cervids. Specifically, we focus on known polymorphisms in the Prnp gene, observed genotypic differences in CWD infection rates and clinical progression, mechanisms for genetic TSE resistance related to both the cervid host and the prion agent and potential for natural selection for CWD-resistance. We also identify gaps in our knowledge that require future research.
Survival and selection
The survival advantage conferred by decreased CWD susceptibility can be sufficient to alter population dynamics and provide selective pressure favoring disease resistance (demonstrated for the 96S allele in white-tailed deer, in press20). Such selective pressure is rarely measurable in wild populations, and indicates the potential for CWD to impact cervid populations. Additional genetic work will be needed to evaluate potential selective pressure on other loci and in other species to understand future trends in CWD epidemics and deer populations. Further, we currently lack information about non-disease related fitness characteristics associated with Prnp genetics. This is fertile ground for future selection studies. Future research such as simulation modeling might be used to address questions of how selective pressure could change as disease prevalence alters infection hazard, as agent strains shift, or how animal movement affects disease dynamics in wildlife populations.
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