The Ustilago maydis Nit2 Homolog Regulates Nitrogen Utilization and Is Required for Efficient Induction of Filamentous Growth
The Ustilago maydis Nit2 Homolog Regulates Nitrogen Utilization and Is Required for Efficient Induction of Filamentous Growth
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DOI：
10.1128/ec.05191-11
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发表时间：
2012-03-01
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影响因子：
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通讯作者：
Voll, Lars M.
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文献类型：
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作者：
Horst, Robin J.;Zeh, Christine;Voll, Lars M.
氮代谢产物阻遏（NCR）是微生物中发现的一种调控策略，在有利氮源存在下限制复杂和不利氮源的利用。在真菌中，这一概念在酵母和丝状子囊菌中得到了最好的研究，其中加塔转录因子Gln 3 p和Gat 1 p（酵母中）和Nit 2/AreA（子囊菌中）构成了NCR的主要正调控因子。一些植物病原真菌的功能性Nit 2同源物在其宿主中完全毒力所需的原因仍然难以捉摸。我们已经确定了在担子菌植物病原体玉米黑粉菌Nit 2同系物，并表明它是一个主要的，但不是唯一的，积极的调节氮利用。通过对生长在缺乏有利氮源的人工培养基上的孢子进行转录组分析，我们发现只有一部分氮响应基因受到Nit 2的调控，包括Gal 4样转录因子Ton 1（Nit 2的靶点）。黑粉菌酸的生物合成不受Nit 2的控制，而氮饥饿诱导的丝状菌生长在很大程度上依赖于功能性Nit 2。nit 2缺失突变体在玉米叶片上的丝状生长启动延迟，并表现出强烈的毒性受损，表明Nit 2是有效启动U.玉米粉
Nitrogen catabolite repression (NCR) is a regulatory strategy found in microorganisms that restricts the utilization of complex and unfavored nitrogen sources in the presence of favored nitrogen sources. In fungi, this concept has been best studied in yeasts and filamentous ascomycetes, where the GATA transcription factors Gln3p and Gat1p (in yeasts) and Nit2/AreA (in ascomycetes) constitute the main positive regulators of NCR. The reason why functional Nit2 homologs of some phytopathogenic fungi are required for full virulence in their hosts has remained elusive. We have identified the Nit2 homolog in the basidiomycetous phytopathogen Ustilago maydis and show that it is a major, but not the exclusive, positive regulator of nitrogen utilization. By transcriptome analysis of sporidia grown on artificial media devoid of favored nitrogen sources, we show that only a subset of nitrogen-responsive genes are regulated by Nit2, including the Gal4-like transcription factor Ton1 (a target of Nit2). Ustilagic acid biosynthesis is not under the control of Nit2, while nitrogen starvation-induced filamentous growth is largely dependent on functional Nit2. nit2 deletion mutants show the delayed initiation of filamentous growth on maize leaves and exhibit strongly compromised virulence, demonstrating that Nit2 is required to efficiently initiate the pathogenicity program of U. maydis.