The regulatory mechanism of rapid lignification for timely anther dehiscence.

Anther dehiscence is a crucial event in plant reproduction, tightly regulated and dependent on the lignification of the anther endothecium. In this study, we investigated the rapid lignification process that ensures timely anther dehiscence in Arabidopsis. Our findings reveal that endothecium lignification can be divided into two distinct phases. During Phase I, lignin precursors are synthesized without polymerization, while Phase II involves simultaneous synthesis of lignin precursors and polymerization. The transcription factors MYB26, NST1/2, and ARF17 specifically regulate the pathway responsible for the synthesis and polymerization of lignin monomers in Phase II. MYB26-NST1/2 is the key regulatory pathway responsible for endothecium lignification, while ARF17 facilitates this process by interacting with MYB26. Interestingly, our results demonstrate that the lignification of the endothecium, which occurs within approximately 26 h, is much faster than that of the vascular tissue. These findings provide valuable insights into the regulation mechanism of rapid lignification in the endothecium, which enables timely anther dehiscence and successful pollen release during plant reproduction.

miR-211 inhibits the proliferation of human breast cancer cell lines through targeting TFAM / 基础医学与临床

Objective To investigate the role of miR-211/TFAM in the regulation of proliferation of breast cancer cells .Methods In the present study , we transfected breast cancer cells with miR-211 mimics or miR-211 inhibitor to achieve miR-211 and detected the expression of miR-211 and the expression level of TFAM proteins in response to miR-211 overexpression or miR-211 silencing;luciferase reporter gene plasmid with or without a six base pairs mutation in the 3′UTR of TFAM ( mut-TFAM/wt-TFAM) were conducted and co-transfected with miR-211 mimics or miR-211 inhibitor, then the change of the luciferase activity was detected;then pcDNA3.1/TFAM plasmid was constructed and co-transfected with miR-211 mimics or miR-211 inhibitor, TFAM protein expression level changes were determined in response to miR-211 overexpression or miR-211 silencing; lastly the cell proliferation was determined in response to mimics NC/miR-211 mimics and pcDNA3.1/TFAM co-transfection.Results Overex-pression of miR-211 inhibits the expression of TFAM protein , miR-211 silencing promote TFAM protein expression;miR-211 can regulate the expression of TFAM by direct targeting;TFAM over expression was achieved by pcDNA3.1/TFAM transfection , and TFAM overe xpression can restore the inhibitory effect of miR-211 on TFAM;miR-211 inhibited the growth and proliferation of breast cancer cells , TFAM can promote the growth and proliferation of breast cancer cells;TFAM restored the inhibitory effect of miR-211 on growth and proliferation of breast cancer cells .Conclusions miR-211 regulates the growth of breast cancer cell with targeting of HMGB .