Abstract
Successful fertilization relies on the production and effective release of viable pollen. Failure of anther opening (dehiscence), results in male sterility, although the pollen may be fully functional. MYB26 regulates the formation of secondary thickening in the anther endothecium, which is critical for anther dehiscence and fertility. Here, we show that although the MYB26 transcript shows expression in multiple floral organs, the MYB26 protein is localized specifically to the anther endothecium nuclei and that it directly regulates two NAC domain genes, NST1 and NST2, which are critical for the induction of secondary thickening biosynthesis genes. However, there is a complex relationship of regulation between these genes and MYB26. Using DEX-inducible MYB26 lines and overexpression in the various mutant backgrounds, we have shown that MYB26 up-regulates both NST1 and NST2 expression. Surprisingly normal thickening and fertility rescue does not occur in the absence of MYB26, even with constitutively induced NST1 and NST2, suggesting an additional essential role for MYB26 in this regulation. Combined overexpression of NST1 and NST2 in myb26 facilitates limited ectopic thickening in the anther epidermis, but not in the endothecium, and thus fails to rescue dehiscence. Therefore, by a series of regulatory controls through MYB26, NST1, NST2, secondary thickening is formed specifically within the endothecium; this specificity is essential for anther opening.
Highlights
Successful fertilization relies on the production and effective release of viable pollen
Previous work has shown that NST2 is expressed predominantly in the anther with some expression in the interfascicular fibers and xylary fibers (Zhong and Ye, 2015), whereas NAC SECONDARY WALL THICKENING PROMOTING FACTOR1 (NST1) is expressed in the anther and other tissues where secondary thickening is observed, where it acts alongside NST3/SECONDARY WALL ASSOCIATED NAC DOMAIN PROTEIN1 (SND1) to regulate secondary wall biosynthesis in these tissues (Mitsuda et al, 2005)
We have shown that expression of NST1/NST2 cannot rescue dehiscence and fertility in the myb26 mutant, demonstrating that the downstream NST1/NST2 factors are insufficient for secondary thickening and that expression of MYB26 and presumably the equivalent regulator in the vegetative tissues is essential for correctly localized secondary thickening formation
Summary
Successful fertilization relies on the production and effective release of viable pollen. By a combination of molecular genetic analysis and mathematical modeling, we have shown that the mechanical control of opening is mediated by the bilayer structure of the mature anther wall (Nelson et al, 2012) This is comprised of an outer epidermal cell layer, whose turgor pressure is related to its hydration, and the endothecial layer, whose walls contain helical secondary thickening that resist stretching and bending. The requirement for endothecium thickening for dehiscence has been demonstrated genetically by mutants of MYB26/MALE STERILE35 (Dawson et al, 1993; Steiner-Lange et al, 2003) and NAC SECONDARY WALL THICKENING PROMOTING FACTOR1 (NST1) and NST2 (Mitsuda et al, 2005). The double mutant nst1snd only has limited thickening within these tissues suggesting that NST2 plays a minor role in the regulation of secondary wall biosynthesis in fibers (Zhong and Ye, 2015)
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