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<p>The involvement of Loose Plant Architecture 1 (LPA1) in regulating plant growth and leaf angle has been previously demonstrated. However, the fundamental genetic background remains unidentified. To further understand the tissue expression profile of the <i>NtLPA1</i> gene, an overexpression vector (pBI121-<i>NtLPA1</i>) was developed and employed to modify tobacco using the leaf disc method genetically. Validation confirmed the generation of transgenic tobacco plants with <i>NtLPA1</i> overexpression. The findings indicated that increased <i>NtLPA1</i> overexpression substantially decreased plant auxin sensitivity and modulated signal transduction and polar transport, significantly reducing leaf angle, diminished leaf area during early and late growth stages, and shortened root length. In summary, <i>NtLPA1</i> augmented tobacco resistance to severe shin disease by modulating the expression of disease-associated genes PBZ1, PR1b, and the growth regulator auxin polar transport factor PIN1.</p>

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NtLPA1 overexpression regulates the growth of tobacco and enhances resistance to blight

  • 期刊论文

  • 发表日期：

    2025年1月9日

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  • Guiqin Shi,
  • Yanxiao Bu,
  • Lei Chi,
  • Xifeng Zhang,
  • Yuqing Meng,
  • Shijie Zhang,
  • Geng Tian

摘要

The involvement of Loose Plant Architecture 1 (LPA1) in regulating plant growth and leaf angle has been previously demonstrated. However, the fundamental genetic background remains unidentified. To further understand the tissue expression profile of the NtLPA1 gene, an overexpression vector (pBI121-NtLPA1) was developed and employed to modify tobacco using the leaf disc method genetically. Validation confirmed the generation of transgenic tobacco plants with NtLPA1 overexpression. The findings indicated that increased NtLPA1 overexpression substantially decreased plant auxin sensitivity and modulated signal transduction and polar transport, significantly reducing leaf angle, diminished leaf area during early and late growth stages, and shortened root length. In summary, NtLPA1 augmented tobacco resistance to severe shin disease by modulating the expression of disease-associated genes PBZ1, PR1b, and the growth regulator auxin polar transport factor PIN1.