Genome-wide characterization and expression analysis of SAUR gene family in Melon (Cucumis melo L.).

MAIN CONCLUSION: We identified 66 melon SAUR genes by bioinformatic analyses. CmSAUR19, 38, 58, 62 genes are specifically expressed in different stages of fruit growth, suggesting their participation in regulating fruit development. Auxin plays a crucial role in plant growth by regulating the multiple auxin response genes. However, in melon (Cucumis melo L.), the functions of the auxin early response gene family SAUR (Small auxin up RNA) genes in fruit development are still poorly understood. Through genome-wide characterization of CmSAUR family in melon, we identified a total of 66 CmSAUR genes. The open reading frames of the CmSAUR genes ranged from 234 to 525 bp, containing only one exon and lacking introns. Chromosomal position and phylogenetic tree analyses found that the two gene clusters in the melon chromosome are highly homologous in the Cucurbitaceae plants. Among the four conserved motifs in CmSAUR proteins, motif 1, motif 2, and motif 3 located in most of the family protein sequences, and motif 4 showed a close correlation with the two gene clusters. The CmSAUR28 and CmSAUR58 genes have auxin response elements located in the promoters, suggesting they may be involved in the auxin signaling pathway to regulate fruit development. Through transcriptomic profiling in the four developmental stages of fruit and different lateral organs, we selected 16 differentially-expressed SAUR genes for performing further expression analyses. qRT-PCR results showed that five SAUR genes are specifically expressed in flower organs and ovaries. CmSAUR19 and CmSAUR58 were significantly accumulated in the early developmental stage of the fruit. CmSAUR38 and CmAUR62 showed high expression in the climacteric and post-climacteric stages, suggesting their specific role in controlling fruit ripening. This work provides a foundation for further exploring the function of the SAUR gene in fruit development.

Voltage-gated sodium channels ß3 subunit promotes tumorigenesis in hepatocellular carcinoma by facilitating p53 degradation.

The voltage-gated sodium channels (VGSCs) are aberrantly expressed in a variety of tumors and play an important role in tumor growth and metastasis. Here, we show that VGSCs auxiliary ß3 subunit, encoded by the SCN3B gene, promotes proliferation and suppresses apoptosis in HepG2 cells by promoting p53 degradation. ß3 significantly increases HepG2 cell proliferation, promotes tumor growth in mouse xenograft models, and suppresses senescence and apoptosis. We found that ß3 knockdown stabilizes p53 protein, leading to potentiation of p53-induced cell cycle arrest, senescence, and apoptosis. Mechanistic studies revealed that ß3 could bind to p53, promoting p53 ubiquitination and degradation by stabilizing the p53/MDM2 complex. Our results suggest that ß3 is a novel negative regulator of p53 and a potential oncogenic factor.