Anti-SHC2 monoclonal antibody, clone 5B5

We have previously found alterations in expression of native myosin isoforms during adaptations to 30 d of stretch-induced hypertrophy in the quail anterior latissimus dorsi muscle (ALD). However, myosin heavy and light chain expression have not been studied during adaptations to stretch. In the current study, expression of myosin heavy and light chains and native myosin isoforms were characterized after placing a weight on one wing of Japanese quail for 0, 7, 14, or 21 d (N = 8 birds . d(-1)). ALD muscle mass was significantly greater at days 14 (67.0 +/- 4.4%) and 21 (70.2 +/- 4.0%) of stretch compared to day 7 (53.6 +/- 2.9%) of stretch. Native slow myosin-2 (SM2) expression increased from 43.1 +/- 1.7% in control muscles to 55 +/- 1.2% in stretch muscles, relative to the total myosin pool. The increase in native SM2 expression (similar to 12%) was observed at all three time points of stretch. In contrast, native slow myosin-1 (SM1) expression significantly decreased from 34.1 +/- 1.7% in the control muscles to 24.6 +/- 1.2% in the stretch muscles, relative to the total myosin pool. There was an increased expression of slow heavy chain-two (SHC2) concurrent with a downregulation of the slow heavy chain-1 (SHC1). There was no change in the relative percentages of either slow or fast myosin Light chains in overloaded muscles at any of the time points following stretch. These results demonstrate that changes in myosin heavy chain expression, but not myosin Light chain expression accompany stretch-induced hypertrophy in the quail ALD.

The neuronally expressed Shc adaptor homolog SCK1/SHC2 gene contains an unusually high number of minisatellites. In humans, twelve different minisatellite sequences are located in introns of SCK1/SHC2 and ten of them are highly polymorphic. Here we used primers developed for humans to screen ten intronic loci of SCK1/SHC2 in chimpanzee and gorilla, and undertook a comprehensive analysis of the genomic sequence to address the evolutionary events driving these variable repeats. All ten loci amplified in chimpanzee and gorilla contained hypervariable and low-variability minisatellites. The human polymorphic locus TR1 was monomorphic in chimpanzee and gorilla, but we detected polymorphic alleles in these apes for the human monomorphic TR7 locus. When we examined the repeat size among these hominoids, there was no consistent variation by length from humans to great apes. In spite of the inconsistent evolutionary dynamics in repeat length variation, exon 16 was highly conserved between humans and great apes. These results suggest that non-coding intronic minisatellites do not show a consistent evolutionary paradigm but evolved with different patterns among each minisatellite locus. These findings provide important insight for minisatellite conservation during hominoid evolution.