ABSTRACT
Waterlogging is a severe abiotic stressor that inhibits crop growth and productivity owing to the decline in the amount of oxygen available to the waterlogged organs. Although melon (Cucumis melo L.) is sensitive to waterlogging, its ability to form adventitious roots facilitates the diffusion of oxygen and allows the plant to survive waterlogging. To provide comprehensive insight into the adventitious rooting in response to waterlogging of melon, global transcriptome changes during this process were investigated. Of the 17,146 genes expressed during waterlogging, 7363 of them were differentially expressed in the pairwise comparisons between different waterlogging treatment time points. A further analysis suggested that the genes involved in sugar cleavage, glycolysis, fermentation, reactive oxygen species scavenging, cell wall modification, cell cycle governing, microtubule remodeling, hormone signals and transcription factors could play crucial roles in the adventitious root production induced by waterlogging. Additionally, ethylene and ERFs were found to be vital factors that function in melon during adventitious rooting. This study broadens our understanding of the mechanisms that underlie adventitious rooting induced by waterlogging and lays the theoretical foundation for further molecular breeding of waterlogging-tolerant melon. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-021-02866-w.
ABSTRACT
BACKGROUND: Besides androgens, estrogens produced in Leydig cells are also crucial for mammalian germ cell differentiation. Transforming growth factor-ß1 (TGF-ß1) is now known to have multiple effects on regulation of Leydig cell function. The objective of the present study is to determine whether TGF-ß1 regulates estradiol (E2) synthesis in adult rat Leydig cells and then to assess the impact of TGF-ß1 on Cx43-based gap junctional intercellular communication (GJIC) between Leydig cells. METHODOLOGY/PRINCIPAL FINDINGS: Primary cultured Leydig cells were incubated in the presence of recombinant TGF-ß1 and the production of E2 as well as testosterone (T) were measured by RIA. The activity of P450arom was addressed by the tritiated water release assay and the expression of Cyp19 gene was evaluated by Western blotting and real time RT-PCR. The expression of Cx43 and GJIC were investigated with immunofluorescence and fluorescence recovery after photo-bleaching (FRAP), respectively. Results from this study show that TGF-ß1 down-regulates the level of E2 secretion and the activity of P450arom in a dose-dependent manner in adult Leydig cells. In addition, the expression of Cx43 and GJIC was closely related to the regulation of E2 and TGF-ß1, and E2 treatment in turn restored the inhibition of TGF-ß1 on GJIC. CONCLUSIONS: Our results indicate, for the first time in adult rat Leydig cells, that TGF-ß1 suppresses P450arom activity, as well as the expression of the Cyp19 gene, and that depression of E2 secretion leads to down-regulation of Cx43-based GJIC between Leydig cells.
