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Title: Rebirth and death: Nitric oxide and reactive oxygen species in seed

Author
item Bethke, Paul
item LIBOUREL, IGOR - MICHIGAN STATE UNIV
item JONES, RUSSELL - UNIV OF CALIFORNIA

Submitted to: Comparative Biochemistry and Physiology
Publication Type: Abstract Only
Publication Acceptance Date: 1/26/2007
Publication Date: 4/1/2007
Citation: Bethke, P.C., Libourel, I., Jones, R. 2007. Rebirth and death: Nitric oxide and reactive oxygen species in seed [abstract]. Comparative Biochemistry and Physiology. 146(4):S56.

Interpretive Summary:

Technical Abstract: Plant seeds provide excellent opportunities to study well-defined progressions of physiological changes at the single cell, tissue and whole organism levels. Most seeds are dormant at maturity, and dormancy must be lost before germination can occur. The emergence of the embryo and its early growth depend on the coordinated activities of the embryo itself and the tissues surrounding it. We have used Arabidopsis seeds and barley grains to study the roles of plant hormones, nitric oxide (NO), and reactive oxygen species in dormancy loss, germination and post-germinative growth. Our data support the following sequence of events for dormancy and germination in these species. (1) NO produced by the seed is perceived by the aleurone layer, a tissue that surrounds the embryo, and NO-perception promotes dormancy loss. (2) NO perception leads to the transcription in the embryo of genes for the biosynthesis of the plant hormone GA. (3) GA produced by the embryo up regulates the conversion of stored lipid to sugar in the embryo and aleurone. This nourishes the embryo and provides substrates in the aleurone layer for the synthesis and secretion of hydrolytic enzymes. (4) Cell wall degrading hydrolases weaken the aleurone cell wall and allow the embryonic root to break through. (4) Hydrogen peroxide is generated as a by-product of lipid breakdown. In barley GA represses the production of enzymes that metabolize reactive oxygen species. (5) Aleurone cell death occurs as a result of reactive oxygen species damage, but NO acts as an antioxidant and delays death.