Shaulsky G, Kuspa A, Loomis W F
Department of Biology, University of California, San Diego, La Jolla 92093, USA.
Genes Dev. 1995 May 1;9(9):1111-22. doi: 10.1101/gad.9.9.1111.
The prestalk-specific gene, tagB, was disrupted by restriction enzyme-mediated integration (REMI) mutagenesis. Mutant aggregates exhibit a cell-autonomous defect in specialization of PST-A cells, a prestalk subpopulation that forms the tip and eventually forms the stalk of the fruiting body. Cooperative (non-cell-autonomous) defects were found in sporulation and in specialization of prestalk cells that eventually form the upper cup of the fruiting body (PST-O). The pattern of ecmA::lacZ expression in mutant tagB- cells defines a primary prestalk population, PST-I, from which other prestalk cells differentiate. After PST-A cells differentiate, they induce remaining PST-I cells to become PST-O cells. Subsequently, prestalk cells induce encapsulation of prespore cells during culmination. tagB is homologous to serine protease and to multidrug resistance (MDR) transporter genes, implying a mechanism of action that includes proteolysis and export of peptide signals. Intercellular communication via TagB may mediate integration of cellular differentiation with morphogenesis.
柄细胞特异性基因tagB通过限制酶介导整合（REMI）诱变被破坏。突变聚集体在PST-A细胞（一种形成子实体顶端并最终形成柄的柄细胞亚群）特化过程中表现出细胞自主缺陷。在孢子形成和最终形成子实体上杯的柄细胞（PST-O）特化过程中发现了协同（非细胞自主）缺陷。突变tagB-细胞中ecmA::lacZ的表达模式定义了一个主要的柄细胞群体PST-I，其他柄细胞从该群体分化而来。PST-A细胞分化后，它们诱导剩余的PST-I细胞成为PST-O细胞。随后，柄细胞在发育成熟过程中诱导前孢子细胞的包囊化。tagB与丝氨酸蛋白酶和多药耐药（MDR）转运蛋白基因同源，这意味着其作用机制包括蛋白水解和肽信号输出。通过TagB进行的细胞间通讯可能介导细胞分化与形态发生的整合。
