Myostatin maps to porcine chromosome 15 by linkage and physical analyses.

Myostatin belongs to the transforming growth factor-beta superfamily, and is expressed specifically in developing and mature skeletal muscle. Myostatin appears to act as a negative regulator of muscle development, since mice with targeted disruption of this gene display a large increase in muscle mass. In this study, the porcine myostatin gene was mapped to chromosome 15q2.

Association of the muscle hypertrophy locus with carcass traits in beef cattle.

A locus near the centromere of bovine chromosome 2 is responsible for muscle hypertrophy (mh) in cattle. The objectives of this study were to refine the genomic region in which the locus resides and to assess the effects of a single copy of the mh allele on carcass and birth traits. Two half-sib families were developed using a Belgian Blue x MARC III (n = 246) or a Piedmontese x Angus (n = 209) sire.

Comparative mapping of human chromosome 2 identifies segments of conserved synteny near the bovine mh locus.

The "double-muscling" (mh) locus has been localized to an interval between the centromere and the microsatellite marker TGLA44 on bovine Chromosome (Chr) 2 (BTA2). We identified segments of conserved synteny that correspond to this region of BTA2 by assigning large genomic clones containing bovine homologs of seven genes from the long arm of human Chr 2 (HSA2q). Polymorphic markers developed from these clones integrated the physical and linkage maps of BTA2 from 2q12 to 2q44 and extended genetic coverage towards the centromere.

Myostatin maps to the interval containing the bovine mh locus.

Myostatin (GDF-8) is a member of the transforming growth factor-beta superfamily and plays a role in muscle growth and development. Mice having targeted disruption of this gene display marked increases in muscle mass, a phenotype similar to the muscular hypertrophy (mh) in several cattle breeds. Physical mapping data developed from YAC clones indicate the bovine myostatin gene lies close to the centromere of bovine Chromosome (Chr) 2 (BTA2) at 2q11, indistinguishable from the cytogenetic location of the mh locus.

A second-generation linkage map of the bovine genome.

We report a bovine linkage map constructed with 1236 polymorphic DNA markers and 14 erythrocyte antigens and serum proteins. The 2990-cM map consists of a sex-specific, X chromosome linkage group and 29 sex-averaged, autosomal linkage groups with an average interval size of 2.5 cM.

A chromosome-specific microdissected library increases marker density on bovine chromosome 1.

Genetic resolution of bovine chromosome 1 (BTA1) linkage group was significantly increased by screening for microsatellite clones a microdissected library constructed from a bovine cell line carrying a t(1;29) translocation. Eighty-five percent of the microsatellites (ms) (46/54) identified were informative in the USDA/MARC mapping population, and 96% of these ms (44/46) linked to BTA1 (LOD > 3.0).

An integrated genetic and physical map of the bovine X chromosome.

Genotypic data for 56 microsatellites (ms) generated from maternal full sib families nested within paternal half sib pedigrees were used to construct a linkage map of the bovine X Chromosome (Chr) (BTX) that spans 150 cM (ave. interval 2.7 cM).

Autogenous regulation of RNA translation and packaging by Rous sarcoma virus Pr76gag.

Unspliced cytoplasmic retroviral RNA in chronically infected cells either is encapsidated by Gag proteins in the manufacture of virus or is used to direct synthesis of Gag proteins. Several models have been suggested to explain the sorting of viral RNA for these two purposes. Here we present evidence supporting a simple biochemical mechanism that accounts for the routing of retroviral RNA.

Effects of the open reading frames in the Rous sarcoma virus leader RNA on translation.

Three short open reading frames (ORFs) reside in the 5' leader of Rous sarcoma virus (RSV) and are conserved in all avian sarcoma-leukosis retroviruses. Both extensions of the lengths of the ORFs and alterations in their initiation codons affect viral replication and gene expression. To determine whether the effects on viral replication were due to translational regulation mediated by the ORFs, we examined translation following mutation of the initiation and termination codons of each of the three ORFs.

Alterations of the three short open reading frames in the Rous sarcoma virus leader RNA modulate viral replication and gene expression.

The Rous sarcoma virus (RSV) leader RNA has three short open reading frames (ORF1 to ORF3) which are conserved in all avian sarcoma-leukosis retroviruses. Effects on virus propagation were determined following three types of alterations in the ORFs: (i) replacement of AUG initiation codons in order to prohibit ORF translation, (ii) alterations of the codon context around the AUG initiation codon to enhance translation of the normally silent ORF3, and (iii) elongation of the ORF coding sequences. Mutagenesis of the AUG codons for ORF1 and ORF2 (AUG1 and AUG2) singly or together delayed the onset of viral replication and cell transformation.