Tahirovic Sabina, Schorr Markus, Then Angela, Berger Jürgen, Schwarz Heinz, Mayinger Peter
Zentrum für Molekulare Biologie, Universität Heidelberg, Im Neuenheimer Feld 282, 69120 Heidelberg, Germany.
Curr Genet. 2003 May;43(2):71-8. doi: 10.1007/s00294-003-0380-9. Epub 2003 Mar 7.
Polarized deposition of chitin at the bud neck is essential for cell separation in yeast. Chitin septum biogenesis is catalyzed by two distinct chitin synthase activities encoded by the CHS2 and CHS3 genes. The phosphoinositide phosphatase Sac1p is required for proper trafficking of the Chs3p chitin synthase. sac1 mutants also display a severe synthetic growth defect, with mutations in the SLT2 gene which encodes a MAP kinase involved in cell integrity. We characterized the defect that underlies this genetic interaction and found that sac1 Delta slt2 Delta cells arrest as large-budded cells because they fail to separate at the end of mitosis. This inability to complete cell division appears to be caused by an increased deposition of chitin at the septum area and correlates with a mislocalized accumulation of the Chs2p chitin synthase at the cell periphery. Our data therefore indicate that Sac1p and Slt2p have synergistic roles in regulating chitin septum biogenesis.
几丁质在芽颈处的极化沉积对于酵母细胞的分离至关重要。几丁质隔膜的生物合成由CHS2和CHS3基因编码的两种不同的几丁质合酶活性催化。磷酸肌醇磷酸酶Sac1p是Chs3p几丁质合酶正确运输所必需的。sac1突变体还表现出严重的合成生长缺陷，与编码参与细胞完整性的丝裂原活化蛋白激酶的SLT2基因发生突变有关。我们对这种遗传相互作用背后的缺陷进行了表征，发现sac1Δslt2Δ细胞作为大芽细胞停滞，因为它们在有丝分裂末期无法分离。这种无法完成细胞分裂似乎是由于几丁质在隔膜区域的沉积增加所致，并且与Chs2p几丁质合酶在细胞周边的错误定位积累相关。因此，我们的数据表明Sac1p和Slt2p在调节几丁质隔膜生物合成中具有协同作用。
