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Defect in peroxisomal multifunctional enzyme MFE1 affects cAMP relay in Dictyostelium

机译:过氧化物酶体多功能酶MFE1的缺陷会影响网盘菌中的cAMP传递

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We have previously reported that cells of Dictyostelium discoideum lacking the fatty acid oxidation enzyme MFE1 accumulate excess cyclopropane fatty acids from ingested bacteria. Cells in which mfeA(-) is disrupted fail to develop when grown in association with bacteria but form normal fruiting bodies when grown in axenic media. Bacterially grown mfeA(-) cells express the genes for the cyclic AMP (cAMP) receptor (carA) and adenylyl cyclase (acaA) but fail to respond to a cAMP pulse by synthesis of additional cAMP which normally relays the signal. Moreover, they do not accumulate the adhesion protein, gp80, which is encoded by the cAMP-induced gene, csaA. As a consequence, they do not acquire developmentally regulated EDTA-resistant cell-cell adhesion. When mutant cells are mixed with wild-type cells and allowed to develop together, they co-aggregate and differentiate into both spores and stalk cells. Thus, most of the developmental consequences of excess cyclopropane fatty acids appear to result from impaired cAMP relay.
机译:我们以前曾报道过,缺乏脂肪酸氧化酶MFE1的盘基网柄菌细胞会从摄入的细菌中积累过量的环丙烷脂肪酸。与细菌结合生长时,mfeA(-)被破坏的细胞无法发育,但在轴突培养基中生长时会形成正常的子实体。细菌生长的mfeA(-)细胞表达环状AMP(cAMP)受体(carA)和腺苷酸环化酶(acaA)的基因,但无法通过合成通常传递信号的其他cAMP来响应cAMP脉冲。而且,它们不会积聚由cAMP诱导的基因csaA编码的粘附蛋白gp80。结果,它们没有获得发育调节的抗EDTA的细胞粘附。当突变细胞与野生型细胞混合并一起发育时,它们会共同聚集并分化为孢子和茎细胞。因此,过量的环丙烷脂肪酸的大部分发育结果似乎是由于cAMP继发受损造成的。

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