| First Author | Huang QQ | Year | 1999 |
| Journal | J Mol Evol | Volume | 49 |
| Issue | 6 | Pages | 780-8 |
| PubMed ID | 10594179 | Mgi Jnum | J:58719 |
| Mgi Id | MGI:1349520 | Doi | 10.1007/pl00006600 |
| Citation | Huang QQ, et al. (1999) Preserved close linkage between the genes encoding troponin I and troponin T, reflecting an evolution of adapter proteins coupling the Ca(2+) signaling of contractility. J Mol Evol 49(6):780-8 |
| abstractText | Ca(2+)-regulated motility is essential to numerous cellular functions, including muscle contraction. Systems with troponin C, myosin light chain, or calmodulin as the Ca(2+) receptor have evolved in striated muscle and other types of cells to transduce the cytoplasm Ca(2+) signals into allosteric conformational changes of contractile proteins. While these Ca(2+) receptors are homologous proteins, their coupling to the responding elements is quite different in various cell types. The Ca(2+) regulatory system in vertebrate striated muscle represents a highly specialized such signal transduction pathway consisting of the troponin complex and tropomyosin associated with the actin filament. To understand the molecular mechanism in the Ca(2+) regulation of muscle contraction and cell motility, we have revealed a preserved ancestral close linkage between the genes encoding two of the troponin subunits, troponin I and troponin T, in the genome of mouse. The data suggest that the troponin I and troponin T genes may have originated from a single locus and evolved in parallel to encode a striated muscle-specific adapter to couple the Ca(2+) receptor, troponin C, to the actin-myosin contractile machinery. This hypothesis views the three troponin subunits as two structure-function domains: the Ca(2+) receptor and the signal transducing adapter. This model may help to further our understanding of the Ca(2+) regulation of muscle contraction and the structure-function relationship of other potential adapter proteins which are converged to constitute the Ca(2+) signal transduction pathways governing nonmuscle cell motility. |
