The down-regulation of these genes by overexpression of miR319a in jaw-D mutants generates larger leaves with crinkled surfaces owing to the extended cell proliferation along leaf margins ( Palatnik et al., 2003). TCP2, TCP3, TCP4, TCP10, and TCP24 are the targets of miR319a/JAW. Arabidopsis BRANCHED1 ( BRC1) and BRC2, both closely related to the TEOSINTE BRANCHED1 from maize ( Doebley et al., 1997), are involved in suppressing axillary bud outgrowth ( Aguilar-Martinez et al., 2007). A functional analysis shows that the class II TCP genes regulate several aspects of plant development. Duplication and diversification events over millions of years have generated a large family of 24 TCP genes in Arabidopsis of which 11 belong to the class II subfamily ( Martin-Trillo and Cubas, 2010). It is believed that class I TCP genes promote cell division, while class II genes act antagonistically to inhibit cell division ( Li et al., 2005). The TCP members are grouped into two classes based on sequence homology: class I and class II TCPs ( Cubas et al., 1999). The TEOSINTE BRANCHED1, CYCLOIDEA, and PCF ( TCP) family encodes plant-specific transcription factors, which contain a conserved bHLH motif that allows DNA binding and protein–protein interactions ( Cubas et al., 1999 Martin-Trillo and Cubas, 2010). Other genes, such as CA2 (carbonic anhydrase 2), AHP4 ( Arabidopsis histidine-containing phosphotransfer factor 4), SAF1 (secondary wall thickening-associated F-box 1) and CBSX2 (cystathionine β-synthase domain-containing protein), negatively regulate this process, and the overexpression of these genes in Arabidopsis leads to anther non-dehiscent phenotypes ( Jung et al., 2008, 2013 Villarreal et al., 2009 Kim et al., 2012). Mutations in IRREGULAR XYLEM ( IRX) and receptor-like protein kinase 2 ( RPK2) genes also lead to the defective secondary wall thickening of the anther ( Brown et al., 2005 Mizuno et al., 2007 Hao et al., 2014). Overexpression of these two genes results in ectopic secondary thickening in various tissues ( Mitsuda et al., 2005). Two NAC domain transcription factors, NST1 and NST2, function redundantly in regulating endothecium wall thickening and act downstream of MYB26. A loss-of-function mutation of MYB26 disrupts secondary thickening of the anther walls, resulting in non-dehiscent anthers ( Dawson et al., 1999 Steiner-Lange et al., 2003 Yang et al., 2007). The importance of this process has been demonstrated by genetic analysis. Secondary wall thickening of the endothecium generates the tensile force necessary to rupture the stomium and in turn, release the pollen grains ( Keijzer, 1987 Bonner and Dickinson, 1989). Our results suggest that TCP24 acts as an important regulator of secondary cell wall thickening and modulates anther endothecium development.Īnther dehiscence is a multistage process that involves coordinated programmed events in specific cells, including degeneration of the middle layer and the tapetum, thickening of the endothecium, degradation of septum cells, and breakage of stomium cells ( Goldberg et al., 1993 Sanders et al., 1999 Wilson et al., 2011). By contrast, the inhibition of TCP24 using the ectopic expression of a TCP24-SRDX repressor fusion protein, or the silencing of TCP genes by miR319a overexpression, increased cell wall lignification and the enhanced secondary cell wall thickening. Several genes linked to secondary cell wall biogenesis and thickening were down-regulated in these transgenic plants. The overexpression of the miR319a-resistant version of TCP24 in Arabidopsis disrupted the thickening of secondary cell walls in the anther endothecium, leading to male sterility because of arrested anther dehiscence and pollen release. Here, we report that TCP24 negatively regulates secondary wall thickening in floral organs and roots. However, it remains unknown whether these genes are involved in cell wall development. MiR319-targeted TCP genes are believed to regulate cell division in leaves and floral organs. National Key Laboratory of Plant Molecular Genetics, Shanghai Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.Han Wang, Yanfei Mao, Jun Yang and Yuke He *
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