<p><i>Bipolaris sorokiniana</i>, a pathogenic fungus responsible for root rot, crown rot, leaf spot, and black point in wheat, poses a serious threat to both yield and grain quality. To investigate its pathogenic mechanisms, we identified the <i>BsSYT1</i> gene with the Sec7 domain by amplifying the flanking sequence of a T-DNA insertion mutant, BSK-353—which exhibited markedly reduced mycelial growth and attenuated virulence—from a <i>B. sorokiniana</i> mutant library using hiTAIL-PCR. Expression of <i>BsSYT1</i> was significantly upregulated during the infection stage compared to the mycelial stage. Deletion of <i>BsSYT1</i> impaired hyphal growth but unexpectedly enhanced conidiation. Moreover, the Δ<i>BsSYT1</i> mutant exhibited significantly enhanced tolerance to osmotic, oxidative, and cell wall stresses compared to the wild-type strain. Virulence assays demonstrated that while the loss of <i>BsSYT1</i> did not affect appressorium formation, it drastically reduced lesion development on wheat and barley leaves. Furthermore, we identified BsSYT1 as a functional target of the mycotoxin brefeldin A. Collectively, our results establish that <i>BsSYT1</i> is a critical regulator of multiple biological processes in <i>B. sorokiniana</i>, including growth, development, stress responses, and virulence.</p>

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BsSYT1 is required for growth, conidiogenesis, stress response and virulence of Bipolaris sorokiniana

  • Yuehua Geng,
  • Feiyu Yan,
  • Yu Zhang,
  • Mengyao Yang,
  • Changshui Li,
  • Ruilin Shi,
  • Chao Xu,
  • Rui Zang,
  • Qin Guo,
  • Yashuang Guo,
  • Qingzhou Ma,
  • Meng Zhang

摘要

Bipolaris sorokiniana, a pathogenic fungus responsible for root rot, crown rot, leaf spot, and black point in wheat, poses a serious threat to both yield and grain quality. To investigate its pathogenic mechanisms, we identified the BsSYT1 gene with the Sec7 domain by amplifying the flanking sequence of a T-DNA insertion mutant, BSK-353—which exhibited markedly reduced mycelial growth and attenuated virulence—from a B. sorokiniana mutant library using hiTAIL-PCR. Expression of BsSYT1 was significantly upregulated during the infection stage compared to the mycelial stage. Deletion of BsSYT1 impaired hyphal growth but unexpectedly enhanced conidiation. Moreover, the ΔBsSYT1 mutant exhibited significantly enhanced tolerance to osmotic, oxidative, and cell wall stresses compared to the wild-type strain. Virulence assays demonstrated that while the loss of BsSYT1 did not affect appressorium formation, it drastically reduced lesion development on wheat and barley leaves. Furthermore, we identified BsSYT1 as a functional target of the mycotoxin brefeldin A. Collectively, our results establish that BsSYT1 is a critical regulator of multiple biological processes in B. sorokiniana, including growth, development, stress responses, and virulence.