australia maines

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Well-known member
Feb 7, 2007
Hollister, CA
this was interesting.


As everyone knows a group of Aussies are heading off to France for the Centenary of the breed. Below is a copy of the itinery for the conference that will give you an insight into what will be discussed in France.
MONDAY 1/9/08
Reception on the river by the Board of Directors, presentation of the programme on the boat leaving Chateau Gontier or Le Lion d’Angers.
Visit to the Domaine des Rues.
Reception at Chenille Change with local councilors.
TUESDAY 2/9/08
Morning: A theoretical presentation which reviews the application in the breed (Mh), of the genes we would like to use [tenderness, marbling, hornless]
Afternoon: Visit to a herd in control of the Mh gene and a herd in selection of th Mh gene.
Evening: Cellar at Le Layon.
Morning: Blain visit to CRITERE, a presentation on our ability to offer genetic material suitable for export to all countries under every type of health condition.
Afternoon: Visit a farm.
Evening: Cellar of Muscadet.
Morning: Visit to the INRA station of la GRELERAIE and presentation of the ESA research programme.
Afternoon: Visit to SOVIBA, Le Lion d’Angers + St Barthelemy
Evening: Visit to the COINTREAU Museum

not the Mh gene vist.

We have determined the entire myostatin coding sequence for 32 double-muscled cattle sampled from ten European cattle breeds. Seven DNA sequence polymorphisms were identified, of which five would be predicted to disrupt the function of the protein, one is a conservative amino acid substitution, and one a silent DNA sequence variant. Four additional DNA sequence polymorphisms were identified in myostatin intronic sequences. In all but two breeds, all double-muscled animals were either homozygous or compound heterozygotes for one of the five loss-of-function mutations. The absence of obvious loss-of-function mutations in the coding sequence of the two remaining breeds points either towards additional mutations in unexplored segments of the gene, or towards locus heterogeneity of double-muscling.

compound heterozygotes.  wonder if that could be a ccs issue.  interesting that a het with one allele good and one bad with multiple mutations can cause problem.  which is why i am wondering if there is a duplication for ccs and or Mh.

who were some double muscle carriers?