Key message <p>A 2-bp insertion in <i>McLecrk1b</i> encoding an L-type lectin receptor-like kinase (L-LecRLK), the candidate gene for the major QTL <i>mfl5.1</i> for mature fruit length, results in a premature stop codon and causes short fruit in bitter gourd. </p> Abstract <p>Fruit length is a key determinant of yield and market class in bitter gourd, yet the causal genes controlling fruit elongation remain largely unknown. In our previous QTL analysis using two inbred accessions with extremely short (HNU004) and moderately long (HNU025) fruits, <i>mfl5.1</i> showed the largest effect. Here, we applied marker-assisted backcrossing to minimize background effects from additional loci and performed map-based cloning using a large BC<sub>1</sub>F<sub>3</sub> segregating population, which delimited <i>mfl5.1</i> to a 33.84-kb interval containing five genes. Sequence comparison identified a 2-bp insertion in <i>Moc05g28500</i> in HNU004, encoding an L-type lectin receptor-like kinase (McLECRK1b), which introduces a premature stop codon and is predicted to lose the transmembrane and kinase domains. Histological analyses indicated that fruit-length variation is mainly attributable to altered mesocarp cell expansion rather than changes in longitudinal cell layer number. Comparative transcriptome profiling across five stages revealed progressive divergence between long and short fruits, with enrichment of hormone-related processes and cytoskeleton-associated pathways. The truncated McLECRK1b protein displayed altered subcellular localization, and ectopic expression of the wild type and truncated alleles in Arabidopsis exerted opposite effects on silique elongation. Together, these results identify <i>McLECRK1b</i> as the most likely candidate&#xa0;gene underlying <i>mfl5.1</i> and provide insights into the genetic and cellular regulation of fruit elongation in bitter gourd.</p>

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Fine mapping and characterization of the bitter gourd mature fruit-length QTL mfl5.1 reveals a lectin receptor-like kinase gene McLECRK1b controlling fruit elongation

  • Feifan Chen,
  • Jiajun Wei,
  • Yiwei Wen,
  • Daolong Liao,
  • Jiayu Liu,
  • Xuzhen Li,
  • Kaihong Hu,
  • Jiayu Guo,
  • Shanming Li,
  • Hongyu Pu,
  • Fanyang Jin,
  • Libo Tian,
  • Sang Shang

摘要

Key message

A 2-bp insertion in McLecrk1b encoding an L-type lectin receptor-like kinase (L-LecRLK), the candidate gene for the major QTL mfl5.1 for mature fruit length, results in a premature stop codon and causes short fruit in bitter gourd.

Abstract

Fruit length is a key determinant of yield and market class in bitter gourd, yet the causal genes controlling fruit elongation remain largely unknown. In our previous QTL analysis using two inbred accessions with extremely short (HNU004) and moderately long (HNU025) fruits, mfl5.1 showed the largest effect. Here, we applied marker-assisted backcrossing to minimize background effects from additional loci and performed map-based cloning using a large BC1F3 segregating population, which delimited mfl5.1 to a 33.84-kb interval containing five genes. Sequence comparison identified a 2-bp insertion in Moc05g28500 in HNU004, encoding an L-type lectin receptor-like kinase (McLECRK1b), which introduces a premature stop codon and is predicted to lose the transmembrane and kinase domains. Histological analyses indicated that fruit-length variation is mainly attributable to altered mesocarp cell expansion rather than changes in longitudinal cell layer number. Comparative transcriptome profiling across five stages revealed progressive divergence between long and short fruits, with enrichment of hormone-related processes and cytoskeleton-associated pathways. The truncated McLECRK1b protein displayed altered subcellular localization, and ectopic expression of the wild type and truncated alleles in Arabidopsis exerted opposite effects on silique elongation. Together, these results identify McLECRK1b as the most likely candidate gene underlying mfl5.1 and provide insights into the genetic and cellular regulation of fruit elongation in bitter gourd.