PMID- 10594179
OWN - NLM
STAT- MEDLINE
DCOM- 20000106
LR  - 20190905
IS  - 0022-2844 (Print)
IS  - 0022-2844 (Linking)
VI  - 49
IP  - 6
DP  - 1999 Dec
TI  - 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.
PG  - 780-8
AB  - 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.
FAU - Huang, Q Q
AU  - Huang QQ
AD  - Department of Physiology and Biophysics, Case Western Reserve University School
      of Medicine, 10900 Euclid Avenue, Cleveland, OH 44106-4970, USA.
FAU - Jin, J P
AU  - Jin JP
LA  - eng
SI  - GENBANK/AF159424
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - J Mol Evol
JT  - Journal of molecular evolution
JID - 0360051
RN  - 0 (Troponin I)
RN  - 0 (Troponin T)
SB  - IM
SB  - S
MH  - Aging
MH  - Animals
MH  - Calcium Signaling/*genetics
MH  - *Evolution, Molecular
MH  - Gene Expression Regulation/genetics
MH  - Genes, Reporter/genetics
MH  - Genetic Linkage/*genetics
MH  - Genome
MH  - Mice
MH  - Models, Genetic
MH  - Molecular Sequence Data
MH  - *Muscle Contraction
MH  - Muscle, Skeletal/embryology/metabolism
MH  - Myocardial Contraction
MH  - Myocardium/metabolism
MH  - Physical Chromosome Mapping
MH  - Promoter Regions, Genetic/genetics
MH  - Structure-Activity Relationship
MH  - Troponin I/*genetics/metabolism
MH  - Troponin T/*genetics/metabolism
EDAT- 1999/12/14 00:00
MHDA- 1999/12/14 00:01
CRDT- 1999/12/14 00:00
PHST- 1999/12/14 00:00 [pubmed]
PHST- 1999/12/14 00:01 [medline]
PHST- 1999/12/14 00:00 [entrez]
AID - JME1953 [pii]
AID - 10.1007/pl00006600 [doi]
PST - ppublish
SO  - J Mol Evol. 1999 Dec;49(6):780-8. doi: 10.1007/pl00006600.