Saito Tamao, Kato Atsushi, Kay Robert R
Department of Biological Sciences, Faculty of Science, Hokkaido University, Sapporo 060-0810, Japan.
Dev Biol. 2008 May 15;317(2):444-53. doi: 10.1016/j.ydbio.2008.02.036. Epub 2008 Feb 29.
The polyketide DIF-1 induces Dictyostelium amoebae to form stalk cells in culture. To better define its role in normal development, we examined the phenotype of a mutant blocking the first step of DIF-1 synthesis, which lacks both DIF-1 and its biosynthetic intermediate, dM-DIF-1 (des-methyl-DIF-1). Slugs of this polyketide synthase mutant (stlB(-)) are long and thin and rapidly break up, leaving an immotile prespore mass. They have approximately 30% fewer prestalk cells than their wild-type parent and lack a subset of anterior-like cells, which later form the outer basal disc. This structure is missing from the fruiting body, which perhaps in consequence initiates culmination along the substratum. The lower cup is rudimentary at best and the spore mass, lacking support, slips down the stalk. The dmtA(-) methyltransferase mutant, blocked in the last step of DIF-1 synthesis, resembles the stlB(-) mutant but has delayed tip formation and fewer prestalk-O cells. This difference may be due to accumulation of dM-DIF-1 in the dmtA(-) mutant, since dM-DIF-1 inhibits prestalk-O differentiation. Thus, DIF-1 is required for slug migration and specifies the anterior-like cells forming the basal disc and much of the lower cup; significantly the DIF-1 biosynthetic pathway may supply a second signal - dM-DIF-1.
聚酮化合物DIF-1可诱导盘基网柄菌属变形虫在培养物中形成柄细胞。为了更好地确定其在正常发育中的作用,我们研究了一个阻断DIF-1合成第一步的突变体的表型,该突变体既缺乏DIF-1及其生物合成中间体dM-DIF-1(去甲基-DIF-1)。这个聚酮合酶突变体(stlB(-))的蛞蝓状幼体又长又细,并且会迅速解体,留下不能移动的前孢子团。它们的前柄细胞比野生型亲本少约30%,并且缺少一部分类似前部的细胞,这些细胞后来形成外部基盘。子实体中缺少这种结构,这可能导致其沿着基质开始发育成熟。最低限度来说,下杯是不发育的,并且缺乏支撑的孢子团会从柄上滑落。dmtA(-)甲基转移酶突变体在DIF-1合成的最后一步被阻断,其与stlB(-)突变体相似,但尖端形成延迟且前柄-O细胞较少。这种差异可能是由于dM-DIF-1在dmtA(-)突变体中的积累,因为dM-DIF-1会抑制前柄-O细胞的分化。因此,DIF-1是蛞蝓状幼体迁移所必需的,并且决定了形成基盘和大部分下杯的类似前部的细胞;重要的是,DIF-1生物合成途径可能会提供第二种信号——dM-DIF-1。