Credit: Kyushu University/Nakayama Lab
Researchers found that a mutation in the ribosomal protein RPL3L, expressed only in heart and skeletal muscle, reduce cardiac contractility in mice. The team found that as the mutant RPL3L reads mRNA it would delay translation for the amino acids proline and alanine. This delay caused ribosomes to collide along the mRNA resulting in misfolded proteins that would be cleared out from the cell. While the deficiency altered translation dynamics for the entire tissue, its effects were most pronounced for proteins related cardiac muscle contraction.