通过逆向遗传学，该课题组人员发现PKS2和PBG13酶在真菌形成炭疽病和稻瘟病的半透性屏障中是必需的。这些酶合成3,5-二羟基己酸聚合物，对致病性至关重要。这些聚合物降低细胞壁的渗透性和产生肿胀，独立于黑色素化。他们的发现揭示了真菌膨胀产生的机制，将酶功能与病原体渗透和疾病潜力联系起来，为疾病控制提供了新的靶点。
据悉，许多植物病原真菌机械地穿透寄主表面，使被称为附着胞的特殊感染细胞产生膨胀压力。这些附着胞发育出半透性细胞壁，并在内部积累渗透物，通过渗透作用产生膨胀。虽然已知黑色素对肿胀的产生很重要，但壁半通透性的机制尚不清楚。
附：英文原文
Title: Dihydroxyhexanoic acid biosynthesis controls turgor in pathogenic fungi
Author: Naoyoshi Kumakura, Takayuki Motoyama, Keisuke Miyazawa, Toshihiko Nogawa, Julien Pernier, Katsuma Yonehara, Mayuko Sato, Yumi Goto, Kaori Sakai, Nobuaki Ishihama, Kaisei Matsumori, Pamela Gan, Kiminori Toyooka, Sandrine Lévêque-Fort, Hiroyuki Koshino, Takeshi Fukuma, Richard J. O’Connell, Ken Shirasu
Issue&Volume: 2026-02-12
Abstract: Many plant pathogenic fungi penetrate host surfaces mechanically, using turgor pressure generated by specialized infection cells called appressoria. These appressoria develop semipermeable cell walls and accumulate osmolytes internally to create turgor by osmosis. Although melanin is known to be important for turgor generation, the mechanism underlying wall semipermeability remains unclear. By using reverse genetics, we identified that the enzymes PKS2 and PBG13 are required for forming the semipermeable barrier in fungi causing anthracnose and rice blast diseases. These enzymes synthesize 3,5-dihydroxyhexanoic acid polymers that are essential for pathogenicity. These polymers reduce cell wall permeability and generate turgor, independently of melanization. Our findings uncover a mechanism of fungal turgor generation, linking enzyme function to pathogen penetration and disease potential, presenting new targets for disease control.
DOI: aec9443
Source: https://www.science.org/doi/10.1126/science.aec9443