4.3 Article

Grain dormancy loss is associated with changes in ABA and GA sensitivity and hormone accumulation in bread wheat, Triticum aestivum (L.)

Journal

SEED SCIENCE RESEARCH
Volume 25, Issue 2, Pages 179-193

Publisher

CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0960258515000057

Keywords

abscisic acid; afterripening; cold stratification; dormancy; gibberellin; pre-harvest sprouting; Triticum aestivum

Categories

Funding

  1. National Science Foundation's East Asia and Pacific Summer Institute Award [1209878]
  2. Japanese Society for Promotion of Science Summer Internship Award
  3. Washington Grain Commission
  4. US Department of Agriculture-Agricultural Research Service
  5. Office Of The Director
  6. Office Of Internatl Science &Engineering [1209878] Funding Source: National Science Foundation

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Knowledge about the hormonal control of grain dormancy and dormancy loss is essential in wheat, because low grain dormancy at maturity is associated with the problem of pre-harvest sprouting (PHS) when cool and rainy conditions occur before harvest. Low GA (gibberellin A) hormone sensitivity and high ABA (abscisic acid) sensitivity were associated with higher wheat grain dormancy and PHS tolerance. Grains of two PHS-tolerant cultivars were very dormant at maturity, and insensitive to GA stimulation of germination. More PHS-susceptible cultivars were less sensitive to ABA inhibition of germination, and were either more GA sensitive or germinated efficiently without GA at maturity. As grain dormancy was lost through dry afterripening or cold imbibition, grains first gained GA sensitivity and then lost ABA sensitivity. These changes in GA and ABA sensitivity can serve as landmarks defining stages of dormancy loss that cannot be discerned without hormone treatment. These dormancy stages can be used to compare different cultivars, seed lots and studies. Previous work showed that wheat afterripening is associated with decreasing ABA levels in imbibing seeds. Wheat grain dormancy loss through cold imbibition also led to decreased endogenous ABA levels, suggesting that reduced ABA signalling is a general mechanism triggering dormancy loss.

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