Development Anatomy in Wheat of Male Sterility Induced by Heat Stress, Water Deficit or Abscisic Acid
HS Saini, M Sedgley and D Aspinall
Australian Journal of Plant Physiology
11(4) 243 - 253
Well watered wheat (Triticum aestivum L. cv. Gabo) plants grown at 20°C were subjected to heat stress (30°C for 3 days), water stress (leaf water potential -2.54 MPa) or exogenous application of abscisic acid (ABA, 3 × 10-5 M) during meiosis in the pollen mother cells. All these treatments caused male sterility. The developmental anatomy of abortive anthers and pollen grains was studied using light microscopy.
The anatomical events leading to pollen abortion in response to heat stress, water stress, and abscisic acid were generally similar. Three developmental sequences leading to sterility were identified. Type 1 was observed in response to heat stress and ABA. Premature tapetal degeneration resulted in periplasmodial invasion of the locule at meiosis and resulted in total sterility. Type 2 was observed in response to water stress when the microspores lost contact with the tapetum at first pollen grain mitosis (PGM I) and the filament degenerated. This also resulted in total sterility. Type 3 was observed in response to all three stresses and led to partial sterility. The microspores completed PGM 1 but a proportion became disoriented from the tapetum and developed no further.
Each stress treatment resulted in two groups of abnormal anther locules, one completely sterile and the other partially sterile. Heat stress and ABA resulted in very similar abnormal development which differed only in the proportion of the two types (1 and 3). Water stress produced partial sterility through the same developmental pattern as heat stress and ABA (type 3). The sequence leading to total sterility in water stress affected anthers (type 2) was similar to that resulting in partial sterility (type 3). The results do not support the hypothesis that ABA is the single primary controlling agent in water stress induced sterility and the question of whether similar mechanisms lead to male sterility in response to the three treatments remains unanswered.
Full text doi:10.1071/PP9840243
© CSIRO 1984