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Key message <p><b>Cotton GhMAX2 positively regulates fiber elongation by mediating the degradation of GhS1FA, which transcriptionally represses GhKCS9 expression.</b></p> Abstract <p>Strigolactones (SLs) are known to promote cotton fiber development. However, the precise molecular relationship between SL signaling and fiber cell elongation remains unclear. In this study, we investigate the role of F-box E3 ligase MORE AXILLARY GROWTH2 (MAX2) in upland cotton in relation to the regulation of fiber development. GhMAX2b and GhMAX2f act as key components for SL signal transduction, with their loss-of-function leading to a notable reduction in fiber length. Biochemical analysis showed that GhMAX2b/f trigger the ubiquitination and subsequent degradation of the transcription repressor strigolactone-1-factor-At (GhS1FA), which function as a substrate for these E3 ligases. Furthermore, GhS1FA inhibits fatty acids biosynthesis by directly binding to the W-box element within the promoter of <i>3</i>-<i>ketoacyl</i>-<i>CoA synthases 9</i> (<i>GhKCS9</i>) and repressing its expression. In summary, we propose that GhMAX2b/f promote fiber elongation, potentially operating partially independently of GhD53 degradation.</p>

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Cotton GhMAX2 promotes single-celled fiber elongation by releasing the GhS1FA-mediated inhibition of fatty acid biosynthesis

  • 期刊论文

  • 发表日期：

    2025年1月10日

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  • Yaru Sun,
  • Shuangxia Jin,
  • Guoli Song

摘要

Key message

Cotton GhMAX2 positively regulates fiber elongation by mediating the degradation of GhS1FA, which transcriptionally represses GhKCS9 expression.

Abstract

Strigolactones (SLs) are known to promote cotton fiber development. However, the precise molecular relationship between SL signaling and fiber cell elongation remains unclear. In this study, we investigate the role of F-box E3 ligase MORE AXILLARY GROWTH2 (MAX2) in upland cotton in relation to the regulation of fiber development. GhMAX2b and GhMAX2f act as key components for SL signal transduction, with their loss-of-function leading to a notable reduction in fiber length. Biochemical analysis showed that GhMAX2b/f trigger the ubiquitination and subsequent degradation of the transcription repressor strigolactone-1-factor-At (GhS1FA), which function as a substrate for these E3 ligases. Furthermore, GhS1FA inhibits fatty acids biosynthesis by directly binding to the W-box element within the promoter of 3-ketoacyl-CoA synthases 9 (GhKCS9) and repressing its expression. In summary, we propose that GhMAX2b/f promote fiber elongation, potentially operating partially independently of GhD53 degradation.