Damveld Robbert A, Arentshorst Mark, Franken Angelique, vanKuyk Patricia A, Klis Frans M, van den Hondel Cees A M J J, Ram Arthur F J
Institute of Biology, Leiden University, Clusius Laboratory, Fungal Genetics Research Group, Wassenaarseweg 64, 2333 AL, Leiden, the Netherlands.
Mol Microbiol. 2005 Oct;58(1):305-19. doi: 10.1111/j.1365-2958.2005.04827.x.
In Aspergillus niger, the genes coding for glutamine:fructose-6-phosphate amidotransferase (gfaA) and alpha-1,3-glucan synthase (agsA) are induced in response to cell wall stress. In silico analysis of the promoter region of the two genes revealed the presence of putative DNA binding sites for transcription factors involved in stress responses, including sites identical to the Saccharomyces cerevisiae Rlm1p and Msn2p/Msn4p transcription factors. Promoter analysis indicated that the induction of the agsA gene in response to cell wall stress is fully dependent on a putative Rlm1p binding site in its promoter region. Database searches revealed the presence of S. cerevisiae Rlm1p homologues in most filamentous fungi examined, including A. niger. Deletion of the RLM1 homologue, named rlmA in A. niger, completely eliminated the induction of agsA and resulted in a twofold reduced induction of gfaA during Calcofluor White-induced cell wall stress. The rise in cell wall chitin in the presence of Calcofluor White was also affected in the rlmA deletion strain. In addition, the deletion strain was more sensitive towards cell wall stress agents. Our results indicate that A. niger responds to cell wall stress by transcriptional activation of cell wall reinforcing genes including agsA and gfaA through an Rlm1p-like transcription factor. We propose that such a cell wall salvage mechanism is wide spread in filamentous fungi.
在黑曲霉中，编码谷氨酰胺：果糖-6-磷酸酰胺转移酶（gfaA）和α-1,3-葡聚糖合酶（agsA）的基因会响应细胞壁应激而被诱导表达。对这两个基因启动子区域的电子分析揭示了存在与应激反应相关的转录因子的假定DNA结合位点，包括与酿酒酵母Rlm1p和Msn2p/Msn4p转录因子相同的位点。启动子分析表明，agsA基因在响应细胞壁应激时的诱导完全依赖于其启动子区域中的一个假定Rlm1p结合位点。数据库搜索显示，在包括黑曲霉在内的大多数被检测丝状真菌中都存在酿酒酵母Rlm1p同源物。在黑曲霉中，名为rlmA的RLM1同源物的缺失完全消除了agsA的诱导，并导致在荧光增白剂诱导的细胞壁应激期间gfaA的诱导降低了两倍。荧光增白剂存在时细胞壁几丁质的增加在rlmA缺失菌株中也受到影响。此外，缺失菌株对细胞壁应激剂更敏感。我们的结果表明，黑曲霉通过一种类似Rlm1p的转录因子对包括agsA和gfaA在内的细胞壁强化基因进行转录激活来响应细胞壁应激。我们提出，这种细胞壁挽救机制在丝状真菌中广泛存在。
