Comparison of locomotion problems and its economic impact on Cobb and Ross broiler strains

The rapid weight gain and fast muscle growth due to intense genetic selection and improved nutrition for additional breast muscle in broiler commercial strains affect chickens health. In order to compare the main locomotive problems in broilers of Cobb and Ross strains, two pens from a commercial farm in Veracruz, Mexico were used. The first pen housed 16,500 males and 16,500 females of Cobb strain and the second one 16,500 males and 16,500 females of Ross strain. Chicks were checked for locomotion problems from day one until their sale. Animals with problems were recorded and necropsies were performed to identify the pathology. Out of 1406 animals with locomotive problems (2.13% of the total), 58.9% were Cobb and 41.1% Ross (P <0.05). The frequency of locomotive problems was 2.51% for Cobb and 1.75% for Ross. Most common individual lesions were osteochondrosis (38.61%), inflamed joints with purulent contents (37.13%), and valgus (19.65%). Locomotive problems appeared since the first week, but its number increased as birds gained weight, particularly from the fourth week on. Problems occurred more in males than in females and in Cobb birds than in the Ross strain. Economic loss due to locomotion problems was higher for the Cobb strain.

LncRNA-FKBP1C regulates muscle fiber type switching by affecting the stability of MYH1B

Long non-coding RNAs (lncRNAs) are well-known to participate in a variety of important regulatory processes in myogenesis. In our previous RNA-seq study (accession number GSE58755), we found that lncRNA-FKBP1C was differentially expressed between White Recessive Rock (WRR) and Xinghua (XH) chicken. Here, we have further demonstrated that lncRNA-FKBP1C interacted directly with MYH1B by biotinylated RNA pull-down assay and RNA immunoprecipitation (RIP). Protein stability and degradation experiments identified that lncRNA-FKBP1C enhanced the protein stability of MYH1B. Overexpression of lncRNA-FKBP1C inhibited myoblasts proliferation, promoted myoblasts differentiation, and participated in the formation of skeletal muscle fibers. LncRNA-FKBP1C could downregulate the fast muscle genes and upregulate slow muscle genes. Conversely, its interference promoted cell proliferation, repressed cell differentiation, and drove the transformation of slow-twitch muscle fibers to fast-twitch muscle fibers. Similar results were observed after knockdown of the MYH1B gene, but the difference was that the MYH1B gene had no effects on fast muscle fibers. In short, these data demonstrate that lncRNA-FKBP1C could bound with MYH1B and enhance its protein stability, thus affecting proliferation, differentiation of myoblasts and conversion of skeletal muscle fiber types.

Synaptic silencing of fast muscle is compensated by rewired innervation of slow muscle

For decades, numerous studies have proposed that fast muscles contribute to quick movement, while slow muscles underlie locomotion requiring endurance. By generating mutant zebrafish whose fast muscles are synaptically silenced, we examined the contribution of fast muscles in both larval and adult zebrafish. In the larval stage, mutants lacked the characteristic startle response to tactile stimuli: bending of the trunk (C-bend) followed by robust forward propulsion. Unexpectedly, adult mutants with silenced fast muscles showed robust C-bends and forward propulsion upon stimulation. Retrograde labeling revealed that motor neurons genetically programmed to form synapses on fast muscles are instead rerouted and innervate slow muscles, which led to partial conversion of slow and intermediate muscles to fast muscles. Thus, extended silencing of fast muscle synapses changed motor neuron innervation and caused muscle cell type conversion, revealing an unexpected mechanism of locomotory adaptation.