Transcription Factor MYB26 Is Key to Spatial Specificity in Anther Secondary Thickening Formation

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.

Copper deficiency alters shoot architecture and reduces fertility of both gynoecium and androecium inArabidopsis thaliana

“…S2). Secondary wall thickening that includes lignification and cellulose deposition, occurs in the endothecium layer in anthers and is essential for anther dehiscence and pollen dispersal (Cecchetti et al, 2013;Hao et al, 2014a;Mitsuda et al, 2005;Yang et al, 2017). Thus, we propose that the entirely abolished anther dehiscence in copper-deficient plants (Fig.…”

A Newly Identified Flower-Specific Splice Variant of AUXIN RESPONSE FACTOR8 Regulates Stamen Elongation and Endothecium Lignification in Arabidopsis

“…The proposed role for ARF8.4 in stamen development is schematically represented in the model shown in Figure 8, where MYB26 transcript is only shown in the endothecium, as this transcript is not functional in the tapetum (Yang et al, 2017). According to this model, the expression of ARF8.4 in the anther endothecium at stages 9 and 10 regulates the timing of endothecium lignification, and ultimately anther dehiscence, by directly activating MYB26.…”

“…Moreover, auxin exerts its effect on anther dehiscence by negatively acting on the expression of MYB26, encoding a transcription factor that controls endothecium lignification, an early event in anther dehiscence that takes place at stage 11. The MYB26 transcript is detectable in the tapetum and endothecium at late stage 10, and MYB26 protein is localized specifically in the anther endothecium nuclei, where it regulates a number of genes linked to secondary thickening (Yang et al, 2007(Yang et al, , 2017. Auxin also negatively controls the biosynthesis of jasmonic acid (JA), which is responsible for stomium opening, the last event of anther dehiscence (Ishiguro et al, 2001;Wilson et al, 2011;Cecchetti et al, 2013).…”

AUXIN RESPONSE FACTOR17 Directly Regulates MYB108 for Anther Dehiscence

“…Moreover, MYB26 directly regulates the expression of NAC SECONDARY WALL THICKEN-ING PROMOTING FACTOR1 (NST1) and NST2. Both myb26 and nst1 nst2 mutants show defective endothelial lignification and failed anther dehiscence (Steiner-Lange et al, 2003;Mitsuda et al, 2005;Yang et al, 2017).…”