Systematic identification and expression analysis of bHLH gene family reveal their relevance to abiotic stress response and anthocyanin biosynthesis in sweetpotato.

BACKGROUND: bHLH transcription factors play significant roles in regulating plant growth and development, stress response, and anthocyanin biosynthesis. Sweetpotato is a pivotal food and industry crop, but little information is available on sweetpotato bHLH genes. RESULTS: Herein, 227 putative IbbHLH genes were defined on sweetpotato chromosomes, and fragment duplications were identified as the dominant driving force for IbbHLH expansion. These IbbHLHs were divided into 26 subfamilies through phylogenetic analysis, as supported by further analysis of exon-intron structure and conserved motif composition. The syntenic analysis between IbbHLHs and their orthologs from other plants depicted evolutionary relationships of IbbHLHs. Based on the transcriptome data under salt stress, the expression of 12 IbbHLHs was screened for validation by qRT-PCR, and differential and significant transcriptions under abiotic stress were detected. Moreover, IbbHLH123 and IbbHLH215, which were remarkably upregulated by stress treatments, had obvious transactivation activity in yeasts. Protein interaction detections and yeast two-hybrid assays suggested an intricate interaction correlation between IbbHLHs. Besides, transcriptome screening revealed that multiple IbbHLHs may be closely related to anthocyanin biosynthesis based on the phenotype (purple vs. white tissues), which was confirmed by subsequent qRT-PCR analysis. CONCLUSIONS: These results shed light on the promising functions of sweetpotato IbbHLHs in abiotic stress response and anthocyanin biosynthesis.

Genome-wide survey and expression analysis of Dof transcription factor family in sweetpotato shed light on their promising functions in stress tolerance.

DNA-binding with one finger (Dof) transcription factors play a crucial role in plant abiotic stress regulatory networks, although massive Dofs have been systematically characterized in plants, they have not been identified in the hexaploid crop sweetpotato. Herein, 43 IbDof genes were detected to be disproportionally dispersed across 14 of the 15 chromosomes of sweetpotato, and segmental duplications were discovered to be the major driving force for the expansion of IbDofs. The collinearity analysis of IbDofs with their related orthologs from eight plants revealed the potential evolutionary history of Dof gene family. Phylogenetic analysis displayed that IbDof proteins were assigned into nine subfamilies, and the regularity of gene structures and conserved motifs was consistent with the subgroup classification. Additionally, five chosen IbDof genes were shown to be substantially and variably induced under various abiotic conditions (salt, drought, heat, and cold), as well as hormone treatments (ABA and SA), according to their transcriptome data and qRT-PCR experiments. Consistently, the promoters of IbDofs contained a number of cis-acting elements associated with hormone and stress responses. Besides, it was noted that IbDof2 had transactivation activity in yeasts, while IbDof-11/-16/-36 did not, and protein interaction network analysis and yeast two-hybrid experiments revealed a complicated interaction connection amongst IbDofs. Collectively, these data lay a foundation for further functional explorations of IbDof genes, especially with regards to the possible application of multiple IbDof members in breeding the tolerant plants.

PKCα/ERK/C7ORF41 axis regulates epidermal keratinocyte differentiation through the IKKα nuclear translocation.

Aberrant differentiation of keratinocytes disrupts the skin barrier and causes a series of skin diseases. However, the molecular basis of keratinocyte differentiation is still poorly understood. In the present study, we examined the expression of C7ORF41 using tissue microarrays by immunohistochemistry and found that C7ORF41 is specifically expressed in the basal layers of skin epithelium and its expression is gradually decreased during keratinocytes differentiation. Importantly, we corroborated the pivotal role of C7ORF41 during keratinocyte differentiation by C7ORF41 knockdown or overexpression in TPA-induced Hacat keratinocytes. Mechanismly, we first demonstrated that C7ORF41 inhibited keratinocyte differentiation mainly through formatting a complex with IKKα in the cytoplasm, which thus blocked the nuclear translocation of IKKα. Furthermore, we also demonstrated that inhibiting the PKCα/ERK signaling pathway reversed the reduction in C7ORF41 in TPA-induced keratinocytes, indicating that C7ORF41 expression could be regulated by upstream PKCα/ERK signaling pathway during keratinocyte differentiation. Collectively, our study uncovers a novel regulatory network PKCα/ERK/C7ORF41/IKKα during keratinocyte differentiation, which provides potential therapeutic targets for skin diseases.

C-Jun/C7ORF41/NF-κB axis mediates hepatic inflammation and lipid accumulation in NAFLD.

Nonalcoholic fatty liver disease (NAFLD) is an expanding health problem worldwide. Although many studies have made great efforts to elucidate the pathogenesis of NAFLD, the molecular basis remains poorly understood. Here, we showed that hepatic C7ORF41, a critical regulator of innate immune response, was markedly decreased in diet or genetic-induced NAFLD model. We also demonstrated that C7ORF41 overexpression significantly ameliorated hepatic inflammation and lipid accumulation in palmitic acid (PA)-treated hepatocytes, whereas C7ORF41 knockdown showed the opposite effects. Mechanistically, we found the anti-inflammatory role of C7ORF41 was attributed to the suppression of NF-κB p65-mediated induction of inflammatory cytokines. Moreover, we demonstrated that the suppression of C7ORF41 expression in hepatocytes is due to JNK activation, which promotes c-Jun-mediated transcriptional repression of C7ORF41. In conclusion, our findings suggested that a c-Jun/C7ORF41/NF-κB regulatory network controls the inflammatory response and lipid accumulation in NAFLD and may benefit the development of novel and promising therapeutic targets for NAFLD.