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环磷酸腺苷是盘基网柄菌中柄细胞分化的一种抑制剂。

Cyclic AMP is an inhibitor of stalk cell differentiation in Dictyostelium discoideum.

作者信息

Berks M, Kay R R

机构信息

MRC Laboratory of Molecular Biology, Cambridge, England.

出版信息

Dev Biol. 1988 Mar;126(1):108-14. doi: 10.1016/0012-1606(88)90244-8.

DOI:10.1016/0012-1606(88)90244-8
PMID:2830156
Abstract

Cyclic AMP and DIF-1 (1-(3,5-dichloro-2,6-dihydroxy-4-methoxyphenyl)-1-hexanone) together induce stalk cell differentiation in vitro in Dictyostelium discoideum strain V12M2. The induction can proceed in two stages: in the first, cyclic AMP brings cells to a DIF-responsive state; in the second, DIF-1 alone can induce stalk cell formation. We report here that during the DIF-1-dependent stage, cyclic AMP is a potent inhibitor of stalk cell differentiation. Addition of cyclic AMP at this stage to V12M2 cells appreciably delays, but does not prevent, stalk cell formation. In contrast, stalk cell differentiation in the more common strain NC4 is completely suppressed by the continued presence of cyclic AMP. This fact explains earlier failures to induce stalk cells in vitro in NC4. We now consistently obtain efficient stalk cell induction in NC4 by removing cyclic AMP in the DIF-1-dependent stage. Cyclic AMP also inhibits the production of a stalk-specific protein (ST310) in both NC4 and a V12M2 derivative. Adenosine, a known antagonist of cyclic AMP action, does not relieve this inhibition by cyclic AMP and does not itself promote stalk cell formation. Finally, stalk cell differentiation of NC4 cells at low density appears to require factors in addition to cyclic AMP and DIF-1, but their nature is not yet known. The inhibition of stalk cell differentiation by cyclic AMP may be important in establishing the prestalk/prespore pattern during normal development, and in preventing the maturation of prestalk into stalk cells until culmination.

摘要

环磷酸腺苷(cAMP)和DIF-1(1-(3,5-二氯-2,6-二羟基-4-甲氧基苯基)-1-己酮)共同作用可在体外诱导盘基网柄菌V12M2菌株的柄细胞分化。这种诱导过程可分为两个阶段:第一阶段,环磷酸腺苷使细胞进入对DIF有反应的状态;第二阶段,单独的DIF-1即可诱导柄细胞形成。我们在此报告,在依赖DIF-1的阶段,环磷酸腺苷是柄细胞分化的有效抑制剂。在此阶段向V12M2细胞中添加环磷酸腺苷会明显延迟但不会阻止柄细胞的形成。相比之下,更常见的NC4菌株中的柄细胞分化会被持续存在的环磷酸腺苷完全抑制。这一事实解释了早期在体外诱导NC4菌株形成柄细胞失败的原因。我们现在通过在依赖DIF-1的阶段去除环磷酸腺苷,始终能在NC4菌株中高效诱导柄细胞形成。环磷酸腺苷还会抑制NC4菌株和V12M2衍生物中一种柄特异性蛋白(ST310)的产生。腺苷是一种已知的环磷酸腺苷作用拮抗剂,它不能解除环磷酸腺苷的这种抑制作用,自身也不能促进柄细胞形成。最后,低密度的NC4细胞的柄细胞分化似乎除了需要环磷酸腺苷和DIF-1外,还需要其他因子,但其性质尚不清楚。环磷酸腺苷对柄细胞分化的抑制作用在正常发育过程中建立前柄/前孢子模式以及防止前柄细胞成熟为柄细胞直至发育成熟方面可能很重要。

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