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褐飞虱操纵水稻糖转运蛋白以利于自身取食。

Brown planthoppers manipulate rice sugar transporters to benefit their own feeding.

机构信息

State Key Laboratory of Rice Biology and Breeding, Key Laboratory of Biology of Crop Pathogens and Insects of Zhejiang Province, Institute of Insect Sciences, Zhejiang University, Hangzhou 310058, China.

Guangdong Provincial Key Laboratory of Applied Botany, South China Botanical Garden, Chinese Academy of Sciences, Guangzhou 510650, China.

出版信息

Curr Biol. 2024 Jul 8;34(13):2990-2996.e4. doi: 10.1016/j.cub.2024.05.028. Epub 2024 Jun 12.

DOI:10.1016/j.cub.2024.05.028
PMID:38870934
Abstract

The feeding of piercing-sucking insect herbivores often elicits changes in their host plants that benefit the insect. In addition to thwarting a host's defense responses, these phloem-feeding insects may manipulate source-sink signaling so as to increase resources consumed. To date, the molecular mechanisms underlying herbivore-induced resource reallocation remain less investigated. Brown planthopper (BPH), an important rice pest, feeds on the phloem and oviposits into leaf sheaths. BPH herbivory increases sugar accumulations 5-fold in the phloem sap of leaf sheaths and concurrently induces the expression of two clade III SWEET genes, SWEET13 and SWEET14, in leaf tissues, but not in leaf sheaths of attacked rice plants. Mutations of both genes by genome editing attenuate resistance to BPH without alterations of known chemical and physical defense responses. Moreover, BPH-elicited sugar levels in the phloem sap were significantly reduced in sweet13/14 mutants, which is likely to attenuate BPH feeding behavior on sweet13/14 mutants. In one of the two field seasons tested, the sweet13/14 mutants showed comparable yield to wild types, and in the other season, the mutants demonstrated stronger BPH resistance. These preliminary results suggested that the mutations in these SWEET transporters could enhance BPH resistance without yield penalties. Given that sweet13/14 mutants also exhibit resistance to bacterial blight pathogen, Xanthomonas oryzae pv. oryzae, these SWEET genes could serve as excellent molecular targets for the breeding of resistant rice cultivars.

摘要

取食穿刺-吸食昆虫的取食常常会引起宿主植物的变化,从而使昆虫受益。除了挫败宿主的防御反应外,这些韧皮部取食昆虫可能会操纵源-库信号,以增加消耗的资源。迄今为止,关于取食诱导的资源再分配的分子机制仍研究较少。褐飞虱(BPH)是一种重要的水稻害虫,以韧皮部为食,并在叶鞘中产卵。BPH 取食使叶鞘韧皮部汁液中的糖分积累增加 5 倍,并同时诱导叶片组织中两个 III 类 SWEET 基因 SWEET13 和 SWEET14 的表达,但在受攻击的水稻植株的叶鞘中没有表达。通过基因组编辑对这两个基因进行突变会削弱对 BPH 的抗性,而不会改变已知的化学和物理防御反应。此外,在 SWEET13/14 突变体中,韧皮部汁液中的 BPH 诱导糖水平显著降低,这可能会削弱 BPH 在 SWEET13/14 突变体上的取食行为。在测试的两个田间季节中的一个中,SWEET13/14 突变体的产量与野生型相当,而在另一个季节,突变体表现出更强的 BPH 抗性。这些初步结果表明,这些 SWEET 转运蛋白的突变可以增强 BPH 抗性,而不会降低产量。鉴于 SWEET13/14 突变体也表现出对细菌性条斑病病原体稻黄单胞菌 pv.oryzae 的抗性,这些 SWEET 基因可以作为培育抗水稻品种的优秀分子靶标。

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