トマトの灰色かび病耐性を強化する転写因子SlERF.F4の発見(Key Transcription Factor SlERF.F4 Found to Strengthen Tomato Resistance to Gray Mold)

2026-04-15 中国科学院(CAS)

本研究は、灰色かび病菌によるトマトの収穫後損失低減に向け、転写因子SlERF.F4の役割を解明したもの。中国科学院武漢植物園の研究チームは、SlERF.F4が成熟緑果に存在し、感染時に発現が増加することを確認した。機能解析では、SlERF.F4を欠損させると感受性が増し、過剰発現で抵抗性が向上することから、本因子が感受性を抑制する役割を持つと示された。さらに、ジャスモン酸シグナルのMYC2により活性化され、PR遺伝子群の誘導や抗酸化酵素の制御を通じてROS恒常性を維持し、防御応答を強化する仕組みが明らかとなった。加えて、果実の成熟や品質に影響を与えず抵抗性を高める点で、育種ターゲットとして有望とされる。

トマトの灰色かび病耐性を強化する転写因子SlERF.F4の発見(Key Transcription Factor SlERF.F4 Found to Strengthen Tomato Resistance to Gray Mold)
Schematic model of SlERF.F4-mediated defense against B. cinerea in tomato fruits (Image by WBG)

<関連情報>

SlERF.F4は、成熟特性とは独立して、トマト果実の灰色かび病菌に対する感受性を負に制御する SlERF.F4 negatively regulates tomato fruit susceptibility to Botrytis cinerea independently of ripening traits

Yu Zhao, Pan Wu, Yulin Huang, Sumin Guo, Xiaofen Yu, Donald Grierson, Lei Gao, Shan Li
Postharvest Biology and Technology  Available online: 6 March 2026
DOI:https://doi.org/10.1016/j.postharvbio.2026.114286

Highlights

  • SlERF.F4 negatively regulates B. cinerea susceptibility per genetic evidence.
  • SlERF.F4 reduces oxidative stress by increasing SOD/POD and decreasing MDA.
  • SlERF.F4 directly activates PR2a and is itself bound and trans-activated by MYC2.
  • SlERF.F4 exerts no effect on ripening and post-harvest fruit quality.

Abstract

Tomato fruits exhibit increased susceptibility to Botrytis cinerea infection during ripening. As a major fungal pathogen affecting tomato production, B. cinerea-induced disease responses are tightly regulated by Ethylene Response Factors (ERFs). SlERF.F4 is highly expressed in tomato fruits at the mature green stage and is strongly induced by B. cinerea infection. Compared with wild-type (WT) fruits, SlERF.F4 knockout (F4-KO) or knockdown (F4-RI) fruits displayed significantly enhanced susceptibility to B. cinerea, whereas SlERF.F4-overexpressing (F4-OE) fruits exhibited slightly reduced susceptibility. Enzymatic activities of superoxide dismutase (SOD) and peroxidase (POD) were decreased in F4-KO and F4-RI fruits but increased in F4-OE fruits relative to WT. In contrast, malondialdehyde (MDA) content showed the opposite trend, suggesting that SlERF.F4 may alleviate oxidative damage in fruits post B. cinerea infection. Genes encoding pathogenesis-related (PR) proteins, including PR2a, CHI1 and PR-STH2 were strongly induced in WT fruits upon B. cinerea infection but expression was impaired in F4-KO fruits, indicating that SlERF.F4 is required for this response. Further, SlERF.F4 could directly bind to the PR2a promoter and trans-activate its expression. Additionally, SlERF.F4 itself is a downstream target of MYC2 in the jasmonic acid (JA) signaling pathway. Notably, no significant differences were observed in days to ripening after anthesis, carotenoid content, firmness, soluble solids content, or postharvest water loss among F4-RI, F4-KO, F4-OE and WT fruits harvested at different ripening stages. In summary, SlERF.F4 induces oxidative-related responses and trans-activates PR gene expression to mitigate susceptibility to B. cinerea infection, without compromising fruit ripening and quality attributes.

1202農芸化学
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