Repressor-AFLR interaction modulates aflatoxin biosynthesis in Aspergillus parasiticus
Repressor-AFLR interaction modulates aflatoxin biosynthesis in Aspergillus parasiticus
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DOI：
10.1023/a:1007157309168
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发表时间：
1999-01-01
期刊：
影响因子：
5.5
通讯作者：
Cleveland, TE
中科院分区：
文献类型：
--
作者：
Chang, PK;Yu, JJ;Cleveland, TE
黄曲霉毒素（AF）的生物合成的调节可能涉及到一个复杂的相互作用的积极和消极的作用因素，受到生理线索响应内部和外部刺激。据推测，这些因子调节AF途径特异性调节基因aflR的表达，aflR的产物AFLR（锌簇转录因子）然后开启或关闭其它AF基因的转录。为了确定AFLR羧基区（AFLRC）是否与正或负作用蛋白相互作用，我们将寄生曲霉aflR羧基编码区（aflRC）融合到A.将niA（p）：：aflRC基因转化A.第2043章.含有两个拷贝的niaA（p）：：aflRC（一个在niaD基因座，另一个在aflR基因座）的转化体过量产生AF前体，而不依赖于氮源。整合的niiA（p）：：aflRC的较高拷贝数与转化体增加的AF前体产生以及aflRC和天然aflR在马铃薯葡萄糖肉汤和A & M培养基中的表达增加相关。由于aflRC不编码DNA结合结构域，因此表达的AFLRC不应结合AF途径基因的启动子并直接影响转录。结果与AFLRC滴定出一个推定的阻遏物，在不同的生长条件下与AFLR相互作用，调节AF的生物合成是一致的。这种相互作用也间接影响了菌核的发育。
Regulation of aflatoxin (AF) biosynthesis likely involves a complex interplay of positive- and negative-acting factors that are affected by physiological cues responsive to internal and external stimuli. These factors, presumably, modulate the expression of the AF pathway-specific regulatory gene, aflR, whose product, AFLR, a zinc cluster transcription factor, then turns on or off the transcription of other AF genes. To determine if the AFLR carboxyl region (AFLRC) interacts with positive- or negative-acting proteins, we fused the Aspergillus parasiticus aflR carboxyl coding region (aflRC) to the promoter of A. parasiticus nitrite reductase gene (niiA(p)::aflRC), and transformed it into A. parasiticus SRRC 2043. Transformants that contained two copies of niiA(p)::aflRC, one at the niaD locus and another at the aflR locus, overproduced AF precursors independent of the nitrogen source. The higher copy number of the integrated niiA(p)::aflRC correlated with increased production of AF precursors by the transformants as well as increased expression of both aflRC and native aflR in potato dextrose broth and A & M medium. Since aflRC does not encode a DNA-binding domain, the expressed AFLRC should not bind to the promoters of AF pathway genes and affect transcription directly. The results are consistent with AFLRC titrating out a putative repressor that interacts with AFLR under different growth conditions and modulates AF biosynthesis. This interaction also indirectly affects sclerotial development.