fluffer
Well-known member
You can't give Karma to yourself is what they ment. (lol)
monkey mouth
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CAB
Well-known member
Power Plant descendants carry Monkey Mouth. We had our 1st visible Monkey Mouth calf this spring.
Hey Barrel Racer, any opinions as to whether or not both parents have to be carrier's for this defect to raises it's head to be visible and are there other side effects besides the visible longer bottom jaw and the shorter top jaw? Just curious as to what the scientific crowd's thoughts are on this one, if you dare. LOL.
Hey Barrel Racer, any opinions as to whether or not both parents have to be carrier's for this defect to raises it's head to be visible and are there other side effects besides the visible longer bottom jaw and the shorter top jaw? Just curious as to what the scientific crowd's thoughts are on this one, if you dare. LOL.
Monkey mouth and parrot mouth are often confused
Monkey mouth is when the bottom jaw sticks out further than the top (ie like the ape impersonations kids do) while parrot mouth is when the top jaw sticks out more than the bottom.
The older literature suggests (this would be before DNA!- it existed, we just didn't know about it) that both are recessive, but since they both have such variable presentations (ie monkey mouth from barely visible to unable to eat) it suggests either several genes involved or variable penetrance. I am not sure anybody really knows and it appears with so many more lethal and perhaps more common defects rearing their ugly heads (like Marble Bone in Red Angus RW and the Long-nosed dwarf in the Angus, not to mention FCS, TH and PHA) it appears to have a low priority in terms of determining the gene or the mutation.
Power Plant is a known carrier of monkey mouth, but I thought Cunia carried parrot mouth - Telos, please correct me if I am wrong!
Monkey mouth is when the bottom jaw sticks out further than the top (ie like the ape impersonations kids do) while parrot mouth is when the top jaw sticks out more than the bottom.
The older literature suggests (this would be before DNA!- it existed, we just didn't know about it) that both are recessive, but since they both have such variable presentations (ie monkey mouth from barely visible to unable to eat) it suggests either several genes involved or variable penetrance. I am not sure anybody really knows and it appears with so many more lethal and perhaps more common defects rearing their ugly heads (like Marble Bone in Red Angus RW and the Long-nosed dwarf in the Angus, not to mention FCS, TH and PHA) it appears to have a low priority in terms of determining the gene or the mutation.
Power Plant is a known carrier of monkey mouth, but I thought Cunia carried parrot mouth - Telos, please correct me if I am wrong!
aj
Well-known member
I could be wrong on cunia but I was always under the impression that cunia's only genetic problem was monkey mouth. Trump goes back to cunia I think.
knabe
Well-known member
i have seen a direct cunia calf with monkey mouth. when i made the list a while ago, i don't remember a single maine bull that passed on monkey mouth that did not have cunia in him.
knabe
Well-known member
the differences in severity of monkey mouth may be due to multiple copy, leading to a dosage effect. this will undoubtably be found out as the cattle genome is sequenced. sadly, repeats of this nature may not be discovered as the cattle genome will not be finished to the same completion level as human. add to this, the complexity of methylation (which can store environmental inputs), and one can easily see that it would be the exception rather than the rule to see consistency and repeatability.
http://www.cmaj.ca/cgi/content/full/176/4/441
In November 2006, however, a new discovery dramatically expanded the understanding of differences between individuals. The publication of the "copy-number variation" (CNV) map of the genome by Steve Scherer's group at Toronto's Sick Children's Hospital and their international collaborators3 initiated a paradigm shift.
The meteoric ascent of CNVs followed from 2 seminal publications in 2004: one from Scherer's group and another from Michael Wigler's group, in Cold Spring Harbor, NY.4,5 Each team used distinct but complementary methods to detect dosage (copy number) differences of chromosomal regions compared with the standard 2 (maternal and paternal) copies that are expected. Both teams saw numerous submicroscopic chromosomal alterations in the genomes of control subjects. These quantitative genomic variants, eventually called CNVs, were analogous to the chromosomal changes detected by classic cytogenetic methods. Whereas SNPs are analogous to a single-letter misprint in a word in an instruction manual, CNVs are analogous to having a page of the manual torn out completely, or pasted in upside down.
The importance of CNVs to human genetic disorders became evident when a search of the map of single-gene disorders showed that almost 300 proven disease-causing genes overlapped with CNVs.5 CNVs can affect phenotypes by altering transcriptional — and presumably translational — levels of genes and their products. For instance, deleting 1 copy of a dosage-sensitive gene results in deficient function that cannot be rescued. CNVs may have a role in polygenic diseases if only for the simplistic reason that certain CNVs span regions containing many genes. Also, genomic deletions in apparently healthy individuals might not directly cause a simple monogenic disease, but in the presence of additional genetic or environmental factors, or both, may contribute to the development later in life of complex polygenic diseases such as diabetes, schizophrenia, cancer and atherosclerosis. Similarly, gene dosage increases are known to cause a few diseases in humans, but the ubiquity of CNVs implies that this could be a more widespread mechanism underlying both rare and common diseases. So the study of SNPs alone when correlating genomic variation with disease is now inadequate in the context of knowledge of CNVs. A focus on SNPs will literally "miss the forest for the trees." For instance, my research group recently showed that testing for both SNPs and CNVs expands the molecular diagnosis of familial hypercholesterolemia.6
http://www.cmaj.ca/cgi/content/full/176/4/441
In November 2006, however, a new discovery dramatically expanded the understanding of differences between individuals. The publication of the "copy-number variation" (CNV) map of the genome by Steve Scherer's group at Toronto's Sick Children's Hospital and their international collaborators3 initiated a paradigm shift.
The meteoric ascent of CNVs followed from 2 seminal publications in 2004: one from Scherer's group and another from Michael Wigler's group, in Cold Spring Harbor, NY.4,5 Each team used distinct but complementary methods to detect dosage (copy number) differences of chromosomal regions compared with the standard 2 (maternal and paternal) copies that are expected. Both teams saw numerous submicroscopic chromosomal alterations in the genomes of control subjects. These quantitative genomic variants, eventually called CNVs, were analogous to the chromosomal changes detected by classic cytogenetic methods. Whereas SNPs are analogous to a single-letter misprint in a word in an instruction manual, CNVs are analogous to having a page of the manual torn out completely, or pasted in upside down.
The importance of CNVs to human genetic disorders became evident when a search of the map of single-gene disorders showed that almost 300 proven disease-causing genes overlapped with CNVs.5 CNVs can affect phenotypes by altering transcriptional — and presumably translational — levels of genes and their products. For instance, deleting 1 copy of a dosage-sensitive gene results in deficient function that cannot be rescued. CNVs may have a role in polygenic diseases if only for the simplistic reason that certain CNVs span regions containing many genes. Also, genomic deletions in apparently healthy individuals might not directly cause a simple monogenic disease, but in the presence of additional genetic or environmental factors, or both, may contribute to the development later in life of complex polygenic diseases such as diabetes, schizophrenia, cancer and atherosclerosis. Similarly, gene dosage increases are known to cause a few diseases in humans, but the ubiquity of CNVs implies that this could be a more widespread mechanism underlying both rare and common diseases. So the study of SNPs alone when correlating genomic variation with disease is now inadequate in the context of knowledge of CNVs. A focus on SNPs will literally "miss the forest for the trees." For instance, my research group recently showed that testing for both SNPs and CNVs expands the molecular diagnosis of familial hypercholesterolemia.6
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