Ultrastructural Characterization of Exine Development of the transient defective exine 1 Mutant Suggests the Existence of a Factor Involved in Constructing Reticulate Exine Architecture from Sporopollenin Aggregates

Abstract

A male-sterile mutant of Arabidopsis thaliana, in which filament elongation was defective although pollen fertility was normal, was isolated by means of T-DNA tagging. Transmission electron microscopy (TEM) analysis revealed that primexine synthesis and probacula formation, which are thought to be the initial steps of exine formation, were defective, and that globular sporopollenin aggregation was randomly deposited onto the microspore at the early uninucleate microspore stage. Sporopollenin aggregation, which failed to anchor to the microspore plasma membrane, was deposited on the locule wall and in the locule at the uninucleate microspore stage. However, visually normal exine with a basic reticulate structure was observed at the middle uninucleate microspore stage, indicating that the exine formation was restored in the mutant. Thus, the mutant was designated transient defective exine 1 (tde1). These results indicated that tde1 mutation affects the initial process of the exine formation, but does not impair any critical processes. Our results also suggest the existence of a certain factor responsible for exine patterning in A. thaliana. The TDE1 gene was found to be identical to the DE-ETIOLATED 2 gene known to be involved in brassinosteroid (BR) biosynthesis, and the tde1 probacula-defective phenotypes were recovered in the presence of BR application. These results suggest that BRs control the rate or efficiency of initial process of exine pattern formation.

Two ATP Binding Cassette G (ABCG) Transporters, OsABCG26 and OsABCG15, Collaboratively Regulate Rice Male Reproduction

“…Although the exact components of the electron-dense granules inclusions observed in osabcg26 are unknown, similar inclusions have been previously described in tapetal locules of Arabidopsis anther lipid metabolism-defective mutants, including a lipid transport mutant atabcg26 (Choi et al, 2011) and three mutants with defective primexine: no exine formation1 (Ariizumi et al, 2004), transient defective exine1 (Ariizumi et al, 2008), and callose synthase5 (Dong et al, 2005). It is believed that primexine is the template for initial sporopollenin accumulation, and defective primexine results in failing sporopollenin deposition, in which feedback regulates the tapetal lipid metabolism (Ariizumi et al, 2004(Ariizumi et al, , 2008Dong et al, 2005;Ariizumi and Toriyama, 2011). Overall, the phenotypic defects of osabcg26 can be explained by the reduced capability to transport lipidic molecules from the tapetum to the endothecium, the epidermis, and the anther surface, which is necessary for normal cuticle formation because of the mutation of OsABCG26.…”

LAP3, a novel plant protein required for pollen development, is essential for proper exine formation

“…Mutants in the TRANSIENT DEFECTIVE EXINE 1 (TDE1) gene delay the development of primexine formation, and the primexine that does form is thin. The mature pollen does, however, form proper exine, albeit its development is delayed (Ariizumi et al 2008).…”

KNS4/UPEX1: A Type II Arabinogalactan β-(1,3)-Galactosyltransferase Required for Pollen Exine Development

“…An Arabidopsis gene, DEFECTIVE IN EXINE FORMATION1 (DEX1), encodes a membrane-associated protein required for primexine development and plasma membrane undulation, and a mutation of the gene results in random deposition of sporopollenin at the plasma membrane surface (Paxson-Sowders et al, 1997;Paxson-Sowders et al, 2001). Mutants of TRANSIENT DEFECTIVE EXINE1 (TDE1)/DE-ETIOLATED2 (DET2) revealed the involvement of brassinosteroids in primexine formation (Ariizumi et al, 2008). The callosic wall in tetrads also plays a crucial role in exine development.…”