Integrated Genetic Mapping, Transcriptomic, and Small RNA Analysis of Fruit Bitterness in Melon
4 affiliations
- 1Key Laboratory of Vegetable Biobreeding, Beijing Vegetable Research Center, Beijing Academy of Agriculture and Forestry Sciences, Beijing 100097, China
- 2College of Horticulture Science and Technology, Hebei Normal University of Science and Technology, Qinhuangdao 066000, China
- 3School of Life Science, Huaibei Normal University, Huaibei 235000, China
- 4Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing 100081, China
Abstract
Melon fruit bitterness, mainly caused by cucurbitacin B (CuB), is a major quality defect that reduces consumer acceptance and market value. However, the genetic and regulatory mechanisms underlying fruit bitterness remain largely unclear. In this study, two thin-skinned melon inbred lines, A54 (bitter leaves and fruit) and B15 (bitter leaves but non-bitter fruit), were used to dissect the genetic basis of fruit bitterness. Genetic analysis revealed that fruit bitterness in A54 is controlled by a single dominant locus. Through bulked-segregant analysis sequencing (BSA-seq) and fine mapping, the candidate region was delimited to a 133-kb interval on chromosome 9, which contains four bHLH genes. Among them, MELO3C005610 (formerly designated CmBr) exhibited 25.5-fold higher expression in A54 than in B15 and was identified as the most plausible positional candidate gene. We further developed a near-isogenic line with bitter fruit (B15NIL) and performed integrated transcriptome, small RNA, and degradome sequencing. Twelve CuB biosynthetic genes were significantly up-regulated in B15NIL fruits, indicating coordinated activation of the cucurbitacin biosynthetic pathway. In addition, small RNA and degradome analyses identified candidate miRNA-target interactions that may contribute to post-transcriptional regulation of CuB biosynthesis, although these interactions require further functional validation. Together, these findings provide a framework for understanding the genetic basis of fruit bitterness in melon and suggest candidate targets for future functional validation and breeding of non-bitter cultivars.
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BibTeX
@article{liu2026integrated,
title = {{Integrated Genetic Mapping, Transcriptomic, and Small RNA Analysis of Fruit Bitterness in Melon}},
author = {Ligong Liu and Guoliang Yuan and Mengqing Lu and Weiqi Han and Haijun Zhang and Jianshe Wang and Huijun Zhang and Congcong Li and Jian Ma},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27209141},
url = {https://www.mdpi.com/1422-0067/27/20/9141},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Integrated Genetic Mapping, Transcriptomic, and Small RNA Analysis of Fruit Bitterness in Melon
AU - Ligong Liu
AU - Guoliang Yuan
AU - Mengqing Lu
AU - Weiqi Han
AU - Haijun Zhang
AU - Jianshe Wang
AU - Huijun Zhang
AU - Congcong Li
AU - Jian Ma
PY - 2026
DA - 2026/10/01
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27209141
UR - https://www.mdpi.com/1422-0067/27/20/9141
AB - Melon fruit bitterness, mainly caused by cucurbitacin B (CuB), is a major quality defect that reduces consumer acceptance and market value. However, the genetic and regulatory mechanisms underlying fruit bitterness remain largely unclear. In this study, two thin-skinned melon inbred lines, A54 (bitter leaves and fruit) and B15 (bitter leaves but non-bitter fruit), were used to dissect the genetic basis of fruit bitterness. Genetic analysis revealed that fruit bitterness in A54 is controlled by a single dominant locus. Through bulked-segregant analysis sequencing (BSA-seq) and fine mapping, the candidate region was delimited to a 133-kb interval on chromosome 9, which contains four bHLH genes. Among them, MELO3C005610 (formerly designated CmBr) exhibited 25.5-fold higher expression in A54 than in B15 and was identified as the most plausible positional candidate gene. We further developed a near-isogenic line with bitter fruit (B15NIL) and performed integrated transcriptome, small RNA, and degradome sequencing. Twelve CuB biosynthetic genes were significantly up-regulated in B15NIL fruits, indicating coordinated activation of the cucurbitacin biosynthetic pathway. In addition, small RNA and degradome analyses identified candidate miRNA-target interactions that may contribute to post-transcriptional regulation of CuB biosynthesis, although these interactions require further functional validation. Together, these findings provide a framework for understanding the genetic basis of fruit bitterness in melon and suggest candidate targets for future functional validation and breeding of non-bitter cultivars.
SN - 1422-0067
ER -