Yamasaki Daiki T, Narita Takaaki B
Graduate School of Engineering, Chiba Institute of Technology, Chiba, Japan.
Department of Life Science, Faculty of Advanced Engineering, Chiba Institute of Technology, Chiba, Japan.
Biosci Biotechnol Biochem. 2024 Oct 22;88(11):1362-1369. doi: 10.1093/bbb/zbae108.
The social amoeba Polysphondylium violaceum uses chemoattractants different from those of Dictyoctelium discoideum for cell aggregation. However, the detailed mechanisms in P. violaceum remain unknown. We have previously reported that the polyketide synthase StlA is involved in inducing aggregation in this species. To elucidate the mechanism of StlA-induced aggregation in P. violaceum, we analyzed the phenotype of P. violaceum stlA- (Pv-stlA-) mutants in more detail. Unlike our previous results, the mutant cells did not exhibit proper chemotaxis toward glorin. Defective aggregation was not restored by glorin pulses, 8Br-cAMP, or deletion of the homologue of PufA that is a translational repressor of protein kinase A, whereas mutant cells grown in the presence of 4-methyl-5-pentylbenzene-1,3-diol (MPBD), the putative Pv-StlA product, aggregated normally without it after starvation. Furthermore, the early developmental marker gene, dscA, was downregulated in the mutant cells. Our data thus suggested that StlA is required for the transition from growth to development in P. violaceum.
群居变形虫紫聚球藻用于细胞聚集的趋化因子与盘基网柄菌不同。然而，紫聚球藻中的详细机制仍不清楚。我们之前报道过聚酮合酶StlA参与诱导该物种的聚集。为了阐明紫聚球藻中StlA诱导聚集的机制，我们更详细地分析了紫聚球藻StlA缺失（Pv-stlA-）突变体的表型。与我们之前的结果不同，突变细胞对光辉霉素没有表现出适当的趋化性。光辉霉素脉冲、8-溴-cAMP或缺失作为蛋白激酶A翻译阻遏物的PufA同源物均不能恢复缺陷聚集，而在假定的Pv-StlA产物4-甲基-5-戊基苯-1,3-二醇（MPBD）存在下生长的突变细胞在饥饿后无需MPBD就能正常聚集。此外，早期发育标记基因dscA在突变细胞中表达下调。因此，我们的数据表明StlA是紫聚球藻从生长向发育转变所必需的。
