| Anther development, the formation of pollen and release is a key stage in plant development, involves more than half of genome gene expression. During pollen development process, the failure of male fertile on the high frequency of mutations can illustrate the degree of genetic intervention. Although the research on male sterile mutants in Arabidopsis thaliana, raised the basic understanding of pollen and anther development, but many aspects of pollen formation is not clear, many faults results in the decrease of fertility or even completely sterile is not typical. In production, some genes related to flower development lead to early flower and fruit of the mechanism is unclear. For those genes with the phenotypic characterization changes in Arabidopsis thaliana and fruit of floral development, we wish to determine their role in pollen and anther development using a variety of physiological and molecular approaches. The results are as follows:ECHIDNA protein impacts on male fertility in arabidopsis by mediating trans-Golgi network secretory trafficking during anther and pollen development. The trans-Golgi network (TGN) plays a central role in cellular secretion and has been implicated in sorting cargo destined for the plasma membrane. Previously, the Arabidopsis(Arabidopsis thaliana) echidna (ech) mutant was shown to exhibit a dwarf phenotype due to impaired cell expansion. However, ech also has a previously uncharacterized phenotype of reduced male fertility. This semisterility is due to decreased anther size and reduced amounts of pollen but also to decreased pollen viability, impaired anther opening, and pollen tube growth. An ECH translational fusion (ECHPro:ECH-YELLOW FLUORESCENT PROTEIN) revealed developmentally regulated tissue-specific expression, with expression in the tapetum during early anther development and microspore release and subsequent expression in the pollen, pollen tube, and stylar tissues. Pollen viability and production, along with germination and pollen tube growth, were all impaired. The ech anther endothecium secondary wall thickening also appeared reduced and disorganized, resulting in incomplete anther opening. In addition, during florescence application of exogenous gibberellic acid (100μM), indole acetic acid (10μM) or jasmonic acid (500μM) did not rescue the ech fertility, it shows that reduced fertility does not contribute to the globe changes in endogenous hormone lever.The ECHPro:ECH-YFP construct was introduced into the myb26 mutant. ECH affects secondary thickening in the endothecium but is not directly associated with the regulation of secondary thickening by MYB26. So this did not appear to be due to anther secondary thickening regulatory genes but perhaps to altered secretion of wall materials through the TGN as a consequence of the absence of the ECH protein. Moreover, the article demonstrated that expression of many genes, which are involved in anther wall formation, pollen development, and anther dehiscence, was altered, although it is largely descriptive with no significant new information provided about the mode of action of ECH. However, it does provide new information uncovering some of the reasons behind the effect of the ech mutation on fertility. The results from this study provided a better understanding of trans-Golgi network trafficking in anther and pollen development. ECH expression is critical for a variety of aspects of male reproduction, including the production of functional pollen grains, their effective release, germination, and tube formation. These stages of pollen development are fundamentally influenced by TGN trafficking of hormones and wall components. Overall, this suggests that the fertility defect is multifaceted, with the TGN trafficking playing a significant role in the process of both pollen formation and subsequent fertilization. |
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