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Cultured myf5 null and myoD null muscle precursor cells display distinct growth defects
Author(s) -
Montarras Didier,
Lindon Catherine,
Pinset Christian,
Domeyne Peggy
Publication year - 2000
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1016/s0248-4900(00)01110-2
Subject(s) - myod , myogenin , myf5 , myocyte , biology , myogenesis , null cell , pitx2 , microbiology and biotechnology , cellular differentiation , myod protein , cell culture , genetics , gene expression , gene , homeobox
Summry— Myf‐5 and MyoD are the two muscle regulatory factors expressed from the myoblast stage to maintain the identity and to promote the subsequent differentiation of muscle precursor cells. To get insight into their role we have studied the capacity to proliferate and to differentiate of myf‐5 and myoD null myoblasts in primary cultures and in the subsequent passages. Our results indicate that myf‐5 null myoblasts differ from wild type (wt) myoblasts in that they undergo precocious differentiation: they become myogenin‐ and troponin T‐positive and fail to incorporate bromodeoxyuridine (BrdU) under culture conditions and at a time when wt cells are not yet differentiated and continue to proliferate. In primary cultures of myoD null cells, up to 60% of the cells were scored as myoblasts on the basis of the expression of myf‐5 . These myoD ‐deficient myoblasts, unlike myoD ‐expressing cells, were poorly differentiating and displayed a severe growth defect that led to their elimination from the cultures: within a few passages myoblasts were absent from myoD ‐deficient cultures, which mostly consisted of senescent cells. That a null mutation in either gene reduces the proliferative potential of cultured myoblasts raises the possibility that Myf‐5 and MyoD serve proliferation of muscle precursor cells.