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对控制聚酮类致病因子T-毒素生物合成的玉米小斑病菌Tox1基因座进行遗传和基因组剖析。

Genetic and genomic dissection of the Cochliobolus heterostrophus Tox1 locus controlling biosynthesis of the polyketide virulence factor T-toxin.

作者信息

Turgeon B Gillian, Baker Scott E

机构信息

Department of Plant Pathology, Cornell University Ithaca, New York 14853, USA.

出版信息

Adv Genet. 2007;57:219-61. doi: 10.1016/S0065-2660(06)57006-3.

Abstract

Fungal pathogenesis to plants is an intricate developmental process requiring biological components found in most fungi, as well as factors that are unique to fungal taxa that participate in particular fungus-plant interactions. The host-selective polyketide toxin known as T-toxin produced by Cochliobolus heterostrophus race T, a highly virulent pathogen of maize, is an intriguing example of the latter type of virulence determinant. The Tox1 locus, which controls biosynthesis of T-toxin, originally defined as a single genetic locus, it is, in fact, two exceedingly complex loci on two chromosomes that are reciprocally translocated with respect to their counterparts in weakly pathogenic race O. Race O lacks the Tox1 locus and does not produce T-toxin. Highly virulent race T was first recognized when it caused an epidemic of Southern Corn Leaf Blight, which devastated the US corn crop in 1970. The evolutionary origin of the Tox1 locus remains unknown.

摘要

真菌对植物的致病作用是一个复杂的发育过程,需要大多数真菌中存在的生物学成分,以及参与特定真菌-植物相互作用的真菌类群所特有的因素。由玉米的高毒力病原菌玉米小斑病菌T小种产生的宿主选择性聚酮化合物毒素T-毒素,就是后一种毒力决定因素的一个有趣例子。控制T-毒素生物合成的Tox1位点最初被定义为一个单一的基因位点,实际上它是位于两条染色体上的两个极其复杂的位点,相对于弱致病性O小种中的对应位点发生了相互易位。O小种缺乏Tox1位点,不产生T-毒素。高毒力的T小种最初是在1970年它引发南方玉米叶枯病流行、使美国玉米作物遭受重创时被发现的。Tox1位点的进化起源仍然未知。

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