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从太阳紫外线损伤中恢复的昆虫病原真菌:分子机制与展望。

Recovery of insect-pathogenic fungi from solar UV damage: Molecular mechanisms and prospects.

机构信息

Institute of Microbiology, College of Life Sciences, Zhejiang University, Hangzhou, P.R. China.

出版信息

Adv Appl Microbiol. 2024;129:59-82. doi: 10.1016/bs.aambs.2024.04.003. Epub 2024 Apr 27.

Abstract

Molecular mechanisms underlying insect-pathogenic fungal tolerance to solar ultraviolet (UV) damage have been increasingly understood. This chapter reviews the methodology established to quantify fungal response to solar UV radiation, which consists of UVB and UVA, and characterize a pattern of the solar UV dose (damage) accumulated from sunrise to sunset on sunny summer days. An emphasis is placed on anti-UV mechanisms of fungal insect pathogens in comparison to those well documented in model yeast. Principles are discussed for properly timing the application of a fungal pesticide to improve pest control during summer months. Fungal UV tolerance depends on either nucleotide excision repair (NER) or photorepair of UV-induced DNA lesions to recover UV-impaired cells in the darkness or the light. NER is a slow process independent of light and depends on a large family of anti-UV radiation (RAD) proteins studied intensively in model yeast but rarely in non-yeast fungi. Photorepair is a rapid process that had long been considered to depend on only one or two photolyases in filamentous fungi. However, recent studies have greatly expanded a genetic/molecular basis for photorepair-dependent photoreactivation that serves as a primary anti-UV mechanism in insect-pathogenic fungi, in which photolyase regulators required for photorepair and multiple RAD homologs have higher or much higher photoreactivation activities than do photolyases. The NER activities of those homologs in dark reactivation cannot recover the severe UV damage recovered by their activities in photoreactivation. Future studies are expected to further expand the genetic/molecular basis of photoreactivation and enrich principles for the recovery of insect-pathogenic fungi from solar UV damage.

摘要

昆虫病原真菌对太阳紫外线 (UV) 损伤的耐受的分子机制已逐渐被理解。本章回顾了定量真菌对太阳 UV 辐射(包括 UVB 和 UVA)响应的方法,并描述了在阳光明媚的夏日从日出到日落期间积累的太阳 UV 剂量(损伤)模式。重点放在昆虫病原真菌的抗 UV 机制与模型酵母中记录的机制进行比较。讨论了在夏季正确应用真菌农药以提高害虫防治效果的原则。真菌的 UV 耐受取决于核苷酸切除修复 (NER) 或光修复 UV 诱导的 DNA 损伤,以在黑暗或光中恢复 UV 损伤的细胞。NER 是一个独立于光的缓慢过程,依赖于大量在模型酵母中深入研究但在非酵母真菌中很少研究的抗 UV 辐射 (RAD) 蛋白。光修复是一个快速过程,长期以来被认为仅依赖于丝状真菌中的一种或两种光解酶。然而,最近的研究极大地扩展了光修复依赖性光复活的遗传/分子基础,它是昆虫病原真菌中的主要抗 UV 机制,在该机制中,光修复所需的光解酶调节剂和多个 RAD 同源物具有比光解酶更高或高得多的光复活活性。那些同源物在暗修复中的 NER 活性不能恢复其在光复活中活性恢复的严重 UV 损伤。预计未来的研究将进一步扩展光复活的遗传/分子基础,并丰富从太阳 UV 损伤中恢复昆虫病原真菌的原则。

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