Kondo Anna P, Narita Takaaki B, Murata Chihiro, Ogura Tetsuhiro, Mikagi Ayame, Usuki Toyonobu, Saito Tamao
Graduate School of Science and Technology, Sophia University, Tokyo, 102-8554, Japan.
Faculty of Science and Technology, Sophia University, Tokyo, 102-8554, Japan.
Curr Microbiol. 2019 Mar;76(3):376-381. doi: 10.1007/s00284-019-01639-2. Epub 2019 Feb 1.
4-Methyl-5-pentylbenzene-1,3-diol (MPBD), a product of the polyketide synthase SteelyA, is a signaling molecule that regulates Dictyostelium discoideum development. During early development, MPBD controls chemotactic cell aggregation by regulating the expression of genes in the cAMP signaling pathway; however, during culmination at late development, it induces spore maturation. In the present study, we analyzed the effects of MPBD, its derivatives, and a putative MPBD-derived metabolite on developmental defects in the MPBD-less stlA null mutant. Using structure-activity relationship studies, it was observed that in MPBD, the functional groups that were essential for induction of spore maturation were different from those essential for induction of cell aggregation. Dictyoquinone, a putative MPBD metabolite rescued the aggregation defect in stlA null mutant in early development, but not the spore maturation defect at the later stage. Our data suggest that MPBD regulates chemotactic cell aggregation and spore maturation via different mechanisms.
4-甲基-5-戊基苯-1,3-二醇（MPBD）是聚酮合酶SteelyA的产物，是一种调节盘基网柄菌发育的信号分子。在早期发育过程中，MPBD通过调节cAMP信号通路中基因的表达来控制趋化性细胞聚集；然而，在发育后期的 culmination 过程中，它诱导孢子成熟。在本研究中，我们分析了MPBD、其衍生物以及一种假定的MPBD衍生代谢物对无MPBD的stlA基因敲除突变体发育缺陷的影响。通过构效关系研究观察到，在MPBD中，诱导孢子成熟所必需的官能团与诱导细胞聚集所必需的官能团不同。Dictyoquinone，一种假定的MPBD代谢物，挽救了早期发育中stlA基因敲除突变体的聚集缺陷，但没有挽救后期的孢子成熟缺陷。我们的数据表明，MPBD通过不同机制调节趋化性细胞聚集和孢子成熟。
