Auxin RegulatesArabidopsisAnther Dehiscence, Pollen Maturation, and Filament Elongation

Abstract

We provide evidence on the localization, synthesis, transport, and effects of auxin on the processes occurring late in Arabidopsis thaliana stamen development: anther dehiscence, pollen maturation, and preanthesis filament elongation. Expression of auxin-sensitive reporter constructs suggests that auxin effects begin in anthers between the end of meiosis and the bilocular stage in the somatic tissues involved in the first step of dehiscence as well as in the microspores and in the junction region between anther and filament. In situ hybridizations of the auxin biosynthetic genes YUC2 and YUC6 suggest that auxin is synthesized in anthers. In agreement with the timing of auxin effects, the TIR1, AFB1, AFB2, and AFB3 auxin receptor-encoding genes are transcribed in anthers only during late stages of development starting at the end of meiosis. We found that in tir1 afb triple and quadruple mutants, anther dehiscence and pollen maturation occur earlier than in the wild type, causing the release of mature pollen grains before the completion of filament elongation. We also assessed the contribution of auxin transport to late stamen developmental processes. Our results suggest that auxin synthesized in anthers plays a major role in coordinating anther dehiscence and pollen maturation, while auxin transport contributes to the independent regulation of preanthesis filament elongation.

Adaptor Protein Complex 2–Mediated Endocytosis Is Crucial for Male Reproductive Organ Development in Arabidopsis

“…In wild-type plants, PIN2:GFP showed stronger signals at the basal PM, indicating that the polar localization of PIN2 at the basal PM may be achieved by the recycling of PIN2 from the PM via endocytosis as observed in root cells (Blilou et al, 2005;Vieten et al, 2007). Consistent with the role of PINs in auxin homeostasis and in filament growth, previous studies have demonstrated that various hormones, in particular auxin, play a crucial role in pollen biogenesis and filament growth, thereby regulating fertilization in Arabidopsis (Cecchetti et al, 2008). Moreover, similar to the ap2m-1 plants, eir1-4 plants, which have loss-of-function mutation in PIN2, showed defects in filament growth and DR5rev:GFP expression in stamens.…”

“…The phenotypes of ap2m-1 plants, in particular, the defects in pollen production and filament elongation, were reminiscent of the phenotypes of yuc2 yuc6, tir1 afb2 afb3, tir1 abf1 abf2 abf3, and arf6 arf8, all of which have a defect in auxin biosynthesis or signaling (Nagpal et al, 2005;Cheng et al, 2006;Cecchetti et al, 2008), raising the possibility that ap2m mutants may also have a defect in maintaining auxin levels. To test whether the failure of pollen elongation is also caused by low levels of auxin, we examined the effect of exogenous auxin application on pollen tube elongation.…”

ER-localized auxin transporter PIN8 regulates auxin homeostasis and male gametophyte development in Arabidopsis

“…On account of its differential distribution within plant tissues, it acts as a versatile coordinative signal mediating a multitude of processes, including female gametophyte patterning, embryogenesis, organogenesis, meristem activity, growth responses to environmental stimuli and others [7][8][9][10] . High auxin concentration in germinating pollen and active auxin responses in developing pollen [11][12][13] implicated auxin also in male gametophyte development and function, but its role there remained elusive.…”

Conversion of Endogenous Indole-3-Butyric Acid to Indole-3-Acetic Acid Drives Cell Expansion in Arabidopsis Seedlings

“…Measurements were made using NIH Image software. comatose alleles of PXA1, the ABC transporter likely to bring IBA into the peroxisome (Zolman et al, 2001b), display a stamen filament elongation delay that is rescued by NAA application (Footitt et al, 2007), suggesting that the auxin required for filament elongation (Cecchetti et al, 2008) is low in this tissue. Similarly, the ibr1 ibr3 ibr10 short-root-hair phenotype was fully rescued by exogenous IAA and NAA, but only partially rescued by the auxin transport inhibitors NPA or TIBA, consistent with the possibility that active auxin levels are low in root hair cells of this mutant.…”