Cold tolerance is a complex trait that requires a critical perspective to understand its underpinning mechanism. To unravel the molecular framework underlying maize (Zea mays L.) cold stress tolerance, we conducted a comparative transcriptome profiling of 24 cold-tolerant and 22 cold-sensitive inbred lines affected by cold stress at the seedling stage. Using the RNA-seq method, we identified 2237 differentially expressed genes (DEGs), namely 1656 and 581 annotated and unannotated DEGs, respectively. Further analysis of the 1656 annotated DEGs mined out two critical sets of cold-responsive DEGs, namely 779 and 877 DEGs, which were significantly enhanced in the tolerant and sensitive lines, respectively. Functional analysis of the 1656 DEGs highlighted the enrichment of signaling, carotenoid, lipid metabolism, transcription factors (TFs), peroxisome, and amino acid metabolism. A total of 147 TFs belonging to 32 families, including MYB, ERF, NAC, WRKY, bHLH, MIKC MADS, and C₂H₂, were strongly altered by cold stress. Moreover, the tolerant lines’ 779 enhanced DEGs were predominantly associated with carotenoid, ABC transporter, glutathione, lipid metabolism, and amino acid metabolism. In comparison, the cold-sensitive lines’ 877 enhanced DEGs were significantly enriched for MAPK signaling, peroxisome, ribosome, and carbon metabolism pathways. The biggest proportion of the unannotated DEGs was implicated in the roles of long non-coding RNAs (lncRNAs). Taken together, this study provides valuable insights that offer a deeper understanding of the molecular mechanisms underlying maize response to cold stress at the seedling stage, thus opening up possibilities for a breeding program of maize tolerance to cold stress.

Gummy stem blight (GSB), caused by Didymella bryoniae, is a devastating fungal disease of melon worldwide. Breeding GSB-resistant cultivars with host resistance genes is considered the most economic and effective strategy to control this disease. In this study, 260 melon germplasm resources were screened for resistance to GSB, and an inbred line, H55R, that exhibited immunity to GSB was identified. To further understand the resistance mechanism of H55R against GSB, an F₂ population was obtained from a cross between the GSB-susceptible line A15 and H55R, and genetic analysis indicated that the GSB resistance in H55R was controlled by a single dominant gene, tentatively named Gsb-7(t). The Gsb-7(t) gene was finally delimited to a 140-kb interval on chromosome 7 using bulked segregant analysis and chromosome walking strategies. Ten putative genes were annotated in this region that contains a wall-associated receptor kinase (WAK) gene MELO3C010403. The MELO3C010403 gene contains two alternative transcripts, MELO3C010403-T1 and MELO3C010403-T2, with five and seven nonsynonymous mutation sites, respectively. Gene expression analysis showed that expression of MELO3C010403-T2 but not MELO3C010403-T1 was significantly induced by D. bryoniae at 24 h postinoculation, indicating that the MELO3C010403-T2 transcript of MELO3C010403 was the most likely candidate gene of Gsb-7(t). Our results offer new genetic resources and will be helpful for the development of GSB-resistant melon cultivars in the future.

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 (B15^NIL) and performed integrated transcriptome, small RNA, and degradome sequencing. Twelve CuB biosynthetic genes were significantly up-regulated in B15^NIL 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.

Deciphering the molecular regulatory networks of panicle development is essential for the genetic improvement of crop yield. However, to date, no systematic studies of gene expression across different panicle developmental stages have been performed in foxtail millet. In this study, a transcriptome analysis of foxtail millet panicle was conducted in four stages of development spanning from the initiation of primary branches to floral organ differentiation. A total of 20,377 expressed genes were identified, including 10,647 differentially expressed genes. Fuzzy C-means clustering detected stage-specific expressed homologs of key transcription regulators, which may be involved in plant organ morphogenesis. Moreover, 1215 transcription factors of 55 families were identified. Members of the MADS-box and GRAS transcription factors showed stage-specific expression patterns, whose conservation was useful in discovering genes related to foxtail millet panicle development. Our analysis was further substantiated by the functional characterization of SiSOC1, whose expression exhibited a gradual upregulation across the four developmental stages. SiSOC1 was identified and validated, which revised the annotation of the reference genome. Overexpression of SiSOC1 markedly accelerated the heading of foxtail millet under long-day and short-day conditions, validating its function in regulating the heading date. In summary, this study systematically identified the transcriptomic landscape of foxtail millet panicle development, and elucidated key regulatory genes. These results provide a theoretical foundation and gene resources for facilitating the molecular breeding of foxtail millet.