librarian
Well-known member
I am still studying the F94L mutation. This is a “conservative” mutation, where there is a substitution of one amino acid with similar function for another. The mutation is non disruptive.
I need some common sense help on a hypothesis concerning Myostatin role in glucose metabolism and some possible lactation energy adaptation rationale for regulatory tweaking during evo-devo. This includes a broader concept of adaptive mutation as non random change, but feedback driven adjustment to energy requirements. https://www.sciencedirect.com/science/article/abs/pii/S1357272510003365
In this paper F94L is Haplotype 1.
https://www.gse-journal.org/articles/gse/pdf/2003/01/g350106.pdf
“ When observing the non-disruptive haplotypes, haplotype 1 appeared in the Aubrac, Limousine and Pirenaica breeds; the latter two breeds were sur- prisingly those in which most individual phenotypes are not explained by a disruptive mutation in the myostatin gene. This indicated a higher pheno- typic influence than expected for a conservative mutation (work currently in progress).”
“ The pattern of haplotype sharing is an indicator of the history of the different bovine populations, or breeds, so the distribution of shared haplotypes is very useful to investigating population relationships. In the last century, different explanations on the origin of the double-muscled phenotype in different contin- ental beef breeds were proposed. One hypothesis is the extensive dissemination of individuals of the Shorthorn breed used in the late 19th century to improve most western European bovine breeds which would explain the presence of the trait [10, 25], and the other being the Friesian breed [9, 20, 31] or more generally milk purpose black pied bovine populations from the Baltic plain (Hanset, pers. comm.), being responsible for spreading the mutation all over western Europe [25].”
I need some common sense help on a hypothesis concerning Myostatin role in glucose metabolism and some possible lactation energy adaptation rationale for regulatory tweaking during evo-devo. This includes a broader concept of adaptive mutation as non random change, but feedback driven adjustment to energy requirements. https://www.sciencedirect.com/science/article/abs/pii/S1357272510003365
In this paper F94L is Haplotype 1.
https://www.gse-journal.org/articles/gse/pdf/2003/01/g350106.pdf
“ When observing the non-disruptive haplotypes, haplotype 1 appeared in the Aubrac, Limousine and Pirenaica breeds; the latter two breeds were sur- prisingly those in which most individual phenotypes are not explained by a disruptive mutation in the myostatin gene. This indicated a higher pheno- typic influence than expected for a conservative mutation (work currently in progress).”
“ The pattern of haplotype sharing is an indicator of the history of the different bovine populations, or breeds, so the distribution of shared haplotypes is very useful to investigating population relationships. In the last century, different explanations on the origin of the double-muscled phenotype in different contin- ental beef breeds were proposed. One hypothesis is the extensive dissemination of individuals of the Shorthorn breed used in the late 19th century to improve most western European bovine breeds which would explain the presence of the trait [10, 25], and the other being the Friesian breed [9, 20, 31] or more generally milk purpose black pied bovine populations from the Baltic plain (Hanset, pers. comm.), being responsible for spreading the mutation all over western Europe [25].”
