GLYCOGEN-SYNTHASE KINASE-3 REGULATES CELL FATE IN DICTYOSTELIUM
GLYCOGEN-SYNTHASE KINASE-3 REGULATES CELL FATE IN DICTYOSTELIUM
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DOI：
10.1016/0092-8674(95)90458-1
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发表时间：
1995-01-13
期刊：
影响因子：
64.5
通讯作者：
KAY, RR
中科院分区：
文献类型：
--
作者：
HARWOOD, AJ;PLYTE, SE;KAY, RR
细胞外环 AMP (cAMP) 诱导盘基网柄菌中前孢子细胞的形成，但抑制茎细胞的形成。我们克隆了 gskA，它编码糖原合酶激酶 3 (GSK-3) 的盘基网柄菌同源物，并发现它是两种 cAMP 作用所必需的。 gskA 的破坏会产生一种突变体，该突变体聚集但形成很少的孢子和异常大量的茎细胞。这些茎细胞可能源自扩大的前茎 B (pstB) 细胞群，该细胞群通常产生子实体的基盘。在培养的突变细胞中，cAMP 既不抑制 pstB 细胞分化，也不诱导有效的前孢子细胞分化。我们认为 cAMP 通过需要 GSK-3 的共同途径发挥作用，并决定前孢子和 pstB 细胞的比例。
Extracellular cyclic AMP (cAMP) induces the formation of prespore cells in Dictyostelium but inhibits stalk cell formation. We have cloned gskA, which encodes the Dictyostelium homolog of glycogen synthase kinase 3 (GSK-3), and discovered that it is required for both cAMP effects. Disruption of gskA creates a mutant that aggregates but forms few spores and an abnormally high number of stalk cells. These stalk cells probably arise from an expanded prestalk B (pstB) cell population, which normally produces the basal disc of the fruiting body. In cultured mutant cells, cAMP neither inhibits pstB cell differentiation nor induces efficient prespore cell differentiation. We propose that cAMP acts through a common pathway that requires GSK-3 and determines the proportion of prespore and pstB cells.