Altered tapetal PCD and pollen wall development in the Arabidopsis ms1 mutant

Abstract

The Arabidopsis male sterility1 mutation results in mature anthers that are devoid of pollen. Meiosis and early development progress normally; however, after microspore release, the microspore cytoplasm and tapetum become abnormally granular and vacuolated, and degeneration occurs. Pollen wall development is seriously affected; primexine formation within the callose wall appears to occur normally, however, once the callose is degraded, abnormal deposits of electrodense material are detected which result in irregular spike-shaped structures, rather than the characteristic rod-like shape of the wild-type bacula. The internal intine wall is also reduced compared with wild type. TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling) staining and ultrastructural analysis have indicated that programmed cell death (PCD) occurs in the wild-type tapetum after microspore mitosis I. However, no signs of PCD are seen in the ms1 tapetum, where large autophagic vacuoles and mitochondrial swelling suggest that necrotic-based breakdown of the tapetum is occurring in the ms1 mutant rather than the normal, regulated PCD process. After the formation of the large, autophagic vacuole in the tapetum, TUNEL staining is detected in the mutant microspores, indicating that they may go through a PCD-based breakdown as a secondary consequence of the observed tapetal aberrations. Based on these observations, two possible roles for MS1 can be hypothesized; MS1 may function by modifying the transcription of tapetal-specific genes implicated in pollen wall development, which then regulate pollen wall material secretion and in turn wall development and tapetal PCD. Alternatively, the MS1 gene may control tapetal development by directly regulating tapetal PCD and breakdown.