Dimitri Pirottin

TL;DR: It is demonstrated that a mutation in bovine MSTN, which encodes myostatin, a member of the TGFβ superfamily, is responsible for the double-muscled phenotype, and an 11-bp deletion in the coding sequence for the bioactive carboxy-termihal domain of the protein causing the muscular hypertrophy observed in Belgian Blue cattle is reported.

TL;DR: It is demonstrated that the GDF8 allele of Texel sheep is characterized by a G to A transition in the 3′ UTR that creates a target site for mir1 and mir206, microRNAs (miRNAs) that are highly expressed in skeletal muscle that causes translational inhibition of the myostatin gene and hence contributes to the muscular hypertrophy ofTexel sheep.

TL;DR: 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.

TL;DR: It is reported that steady-state pulmonary rEos are IL-5-independent parenchymal Siglec-FintCD62L+CD101lo cells with a ring-shaped nucleus, which defines lung rEOS as a distinct eosinophil subset with key homeostatic functions.

TL;DR: It is formally shown that striated muscle is the production site of functional myostatin and that this member of the TGFβ family of growth and differentiation factors regulates muscle mass not only during early embryogenesis but throughout development, indicating that myostarin antagonist could be used to treat muscle wasting and to promote muscle growth in man and animals.