Premium
Role of abscisic acid in perianth senescence of daffodil ( Narcissus pseudonarcissus “Dutch Master”)
Author(s) -
Hunter Donald Alexander,
Ferrante Antonio,
Vernieri Paolo,
Reid Michael Stuart
Publication year - 2004
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.0031-9317.2004.0311.x
Subject(s) - perianth , narcissus , abscisic acid , senescence , botany , horticulture , biology , microbiology and biotechnology , biochemistry , pollen , stamen , gene
Daffodil ( Narcissus pseudonarcissus L. ‘Dutch Master’) flowers detached at the base of their ovaries and held with their cut ends in 10–100 μ M abscisic acid (ABA) senesced prematurely. Symptoms of the ABA treatment included water‐soaking of the tepals and early collapse of the corona. No water‐soaking was seen in tepals of flowers held in water. Instead, the tepals of these flowers dried. The ABA content increased in tepals of the potted flowers as they senesced. The rise in tepal ABA content coincided with the appearance of visual signs of senescence. When the flowers were cut and placed in water, a treatment that accelerated their senescence, the increase in ABA occurred earlier. Exogenously applied ABA enhanced the premature accumulation of senescence‐associated transcripts in the tepals. Their ABA‐mediated induction was not prevented when the flowers were pre‐treated with 1‐methylcyclopropene, an inhibitor of ethylene action, indicating that ABA induced the transcripts independently of ethylene. The transcripts accumulated in opened control flowers before the rise in endogenous ABA. Attempts to extend floral longevity by using putative inhibitors of ABA biosynthesis [tungstate, fluridone (applied as Sonar ® ) and 1,1‐dimethyl‐4‐(phenylsulphonyl)semicarbazide (DPSS)] were unsuccessful. However, inclusion of 100 μ M gibberellic acid (GA 3 ) in the vase solution reduced the senescence‐inducing effects of 50 μ M ABA suggesting a possible mechanism for in‐vivo control of senescence.