二羟基己酸的生物合成控制着病原真菌的张力

Naoyoshi Kumakura, Takayuki Motoyama, Keisuke Miyazawa, Toshihiko Nogawa, Katsuma Yonehara, Kaori Sakai, Nobuaki Ishihama, Kaisei Matsumori, Pamela Gan, Hiroyuki Koshino, Takeshi Fukuma, Richard J. O'Connell, Ken Shirasu
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引用次数: 0

摘要

许多植物病原真菌利用专门的感染细胞--附着体产生的张力压力,以机械方式穿透寄主表面。这些附着体形成半透性细胞壁,并在内部积聚渗透溶质,通过渗透作用产生张力。虽然已知黑色素对产生张力很重要,但细胞壁半透性的机制仍不清楚。在这里,我们通过反向遗传鉴定出 PKS2 和 PBG13 是炭疽病和稻瘟病真菌形成半透膜屏障的关键基因。这些基因编码合成细胞壁特性所必需的 3,5-二羟基己酸聚合物的酶。删除这些酶会损害细胞壁的多孔性,在不影响黑色素形成的情况下降低抗冻性和致病性。我们的发现揭示了一种新的瘤胃生成机制,将酶的功能与病原体的渗透和致病性联系起来,为疾病控制提供了新的目标。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dihydroxyhexanoic acid biosynthesis controls turgor in pathogenic fungi
Many plant pathogenic fungi penetrate host surfaces mechanically, using turgor pressure generated by appressoria, specialized infection cells. These appressoria develop semipermeable cell walls and accumulate osmolytes internally to create turgor by osmosis. While melanin is known to be important for turgor generation, the mechanism for wall semipermeability has remained unclear. Here we identify PKS2 and PBG13, by reverse genetics, as crucial for forming the semipermeable barrier in anthracnose and rice blast fungi. These genes encode enzymes that synthesize 3,5-dihydroxyhexanoic acid polymers essential for the cell wall properties. Deleting these enzymes impairs cell wall porosity, abolishing turgor and pathogenicity without affecting melanization. Our findings uncover a novel mechanism of turgor generation, linking enzyme function to pathogen penetration and disease potential, presenting new targets for disease control.
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