The trichomes of rice leaves are formed by the differentiation and development of epidermal cells.  Plant trichomes play an important role in stress resistance and protection against direct ultraviolet irradiation.  However, the development of rice trichomes remains poorly understood.  In this study, we conducted ethylmethane sulfonate (EMS)-mediated mutagenesis on the wild-type (WT) indica rice ‘Xida 1B’.  Phenotypic analysis led to the screening of a mutant that is defective in trichome development, designated lhl1 (less hairy leaf 1).  We performed map-based cloning and localized the mutated gene to the 70-kb interval between the molecular markers V-9 and V-10 on chromosome 2.  The locus LOC_Os02g25230 was identified as the candidate gene by sequencing.  We constructed RNA interference (LHL1-RNAi) and overexpression lines (LHL1-OE) to verity the candidate gene.  The leaves of the LHL1-RNAi lines showed the same trichome developmental defects as the lhl1 mutant, whereas the trichome morphology on the leaf surface of the LHL1-OE lines was similar to that of the WT, although the number of trichomes was significantly higher.  Quantitative real-time PCR (RT-qPCR) analysis revealed that the expression levels of auxin-related genes and positive regulators of trichome development in the lhl1 mutant were down-regulated compared with the WT.  Hormone response analysis revealed that LHL1 expression was affected by auxin.  The results indicate that the influence of LHL1 on trichome development in rice leaves may be associated with an auxin pathway.

Obesity presents a serious threat to human health and broiler performance.  The expansion of adipose tissue is mainly regulated by the differentiation of preadipocytes.  The differentiation of preadipocytes is a complex biological process regulated by a variety of transcription factors and signaling pathways.  Previous studies have shown that the transcription factor HMG-box protein 1 (HBP1) can regulate the differentiation of mouse 3T3-L1 preadipocytes by activating the Wnt/β-catenin signaling pathway.  However, it is unclear whether HBP1 involved in chicken preadipocyte differentiation and which signaling pathways it regulates.  The aim of the current study was to explore the biological function and molecular regulatory mechanism of HBP1 in the differentiation of chicken preadipocytes.  The expression patterns of chicken HBP1 in abdominal adipose tissue and during preadipocyte differentiation were analyzed by RT-qPCR and Western blot.  The preadipocyte stably overexpressing HBP1 or knockout HBP1 and their control cell line were used to analyze the effect of HBP1 on preadipocyte differentiation by oil red O staining, RT-qPCR and Western blot.  Cignal 45-Pathway Reporter Array was used to screen the signal pathways that HBP1 regulates in the differentiation of chicken preadipocytes.  Chemical inhibitor and siRNA for signal transducer and activator of transcription 3 (STAT3) were used to analyze the effect of STAT3 on preadipocyte differentiation.  The preadipocyte stably overexpressing HBP1 was transfected by the siRNA of STAT3 or treated with a chemical inhibitor of STAT3 for the rescue experiment.  The results of gene expression analysis showed that the expression of HBP1 was related to abdominal fat deposition and preadipocyte differentiation in chickens.  The results of function gain and loss experiments indicated that overexpression/knockout of HBP1 in chicken preadipocytes could inhibit/promote (P<0.05) lipid droplet deposition and the expression of adipogenesis-related genes.  Mechanismlly, HBP1 activates (P<0.05) the signal transducer and activator of transcription 3 (STAT3) signaling pathway by targeting janus kinase 2 (JAK2) transcription.  The results of functional rescue experiments indicated that STAT3 signaling mediated the regulation of HBP1 on chicken preadipocyte differentiation.  In conclusion, HBP1 inhibits chicken preadipocyte differentiation by activating the STAT3 signaling pathway via directly enhancing JAK2 expression.  Our findings provided new insights for further analysis of the molecular genetic basis of chicken adipose tissue growth and development.