The retinoblastoma-like protein p130 is involved in the determination of reserve-cells in differentiating myoblasts

被引:49
作者
Carnac, G
Fajas, L
L'honoré, A
Sardet, C
Lamb, NJC
Fernandez, A
机构
[1] IGH, UPR 1142, Cell Biol Unit, F-34396 Montpellier 5, France
[2] CNRS, UMR 5535, Inst Genet Mol, F-34293 Montpellier, France
关键词
D O I
10.1016/S0960-9822(00)00471-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
During skeletal muscle differentiation, a subset of myoblasts remains quiescent and undifferentiated but retains the capacity to self renew and give rise to differentiating myoblasts [1-3]: this sub-population of muscle cells was recently termed 'reserve cells' [3]. In order to characterise genes that can regulate the ratio between reserve cells and differentiating myoblasts, we examined members of the retinoblastoma tumor suppressor family - Rb, p107 and p130 - an important family of negative regulators of E2F transcription factors and cell cycle progression [4]. Although pRb and p107 positively regulate muscle cell differentiation [5-7], the role of p130 in muscle cells remains unknown. We show here that p130 (protein and mRNA), but neither pRb nor p107, preferentially accumulates during muscle differentiation in reserve cells. Also, p130 is the major Rb-family protein present in E2F complexes in this sub-population of cells. Although forced expression of either p130 or pRb in mouse C2 myoblasts efficiently blocked cell cycle progression, only p130 inhibited the differentiation program. Furthermore, muscle cells overexpressing p130 had reduced levels of the muscle promoting factor MyoD. In addition, p130 repressed the transactivation capacity of MyoD, an effect abolished by co-transfection of pRb, Thus, we propose that p130, by blocking cell cycle progression and differentiation, could be part of a specific pathway that defines a pool of reserve cells during terminal differentiation.
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页码:543 / 546
页数:4
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