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The Biological Role of Abscisic Acid in Precocious Seed Germination. Present by Collin Mecke April 1 st 61.325. Introduction to ABA. -Synthesis of ABA occurs in the chloroplasts and other plastids using the terpenoid pathway (fig 23.2) Detected in all parts of the plant
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The Biological Role of Abscisic Acid in Precocious Seed Germination • Present by Collin Mecke • April 1st • 61.325
Introduction to ABA -Synthesis of ABA occurs in the chloroplasts and other plastids using the terpenoid pathway (fig 23.2) • Detected in all parts of the plant • Transported by both phloem and xylem • Inhibits stomata opening • Regulates seed and bud dormancy
Discovery of ABA • Unknown inhibitory compounds that effect the dormancy of seeds and buds were known about for a long period • Inhibitory compounds that differed from auxin were discovered (1953) • A substance that promotes abscission in cotton fruit was found ten years later and called Abscission II (1963) • At the same time another compound that promoted bud dormancy was found and call Dormin • These two substance (Abscission II and Dormin) were found to be identical and called Abscisic Acid.
How is it Measured? Bioassay-Measuring coleoptile growth inhibition. Minimum detection is 10-7 M -Closure of stomata (10-9M) Physical Methods- Gas Chromatography (10-13g) -High Performance Liquid Chromatography Immunoassay-Recognition of ABA by antibodies (10-13g)
How ABA Causes Dormancy • At high levels of ABA (just before dormancy occurs) late-embyrogenesis abundant proteins (LEA) are produced • LEA’s are thought to be involved in desiccation tolerance • ABA has been shown to affect the amount and composition of storage proteins in a double mutant of Arabidopis (aba/abi3-1) and ABA deficient mutants of maize. • This process is called embryo induced dormancy
Precocious Germination -Immature embryos were removed from seeds and cultured midway through development (before the onset of dormancy) -These embryos germinated precociously (without passing through normal dormancy) - When ABA was added to the medium precocious germination did not occur.
Further Evidence • Zea maize has several mutant species; vp2, vp5 and vp7 that are ABA deficient (fig 23.2) • The embryos of these plants germinate precociously on the cob. This process is called viviparous. • The addition of exogenous ABA prevented precocious germination. • Also, there is a vp1 mutant which is insensitive to ABA. It will germinate precociously even with the addition of exogenous ABA.
Current Research • It has been well documented that the absence of ABA causes precocious germination. • Is a certain amount of GA required? • Fluridone was used to cause ABA deficiency and paclobrutrazol or ancymidol to reduce GA in corn • Measured the amount of GA in each seed and whether precocious germination occurred. • It was found that a minimum amount of GA was required for precocious germination.
Current Research • vp5 maize mutant was cross with a dwarf maize (d1-GA deficient) • The resulting double mutants (vp5/d1) did not undergo precocious germination • Addition of exogenous GA to double mutant did produce precocious germination
Current Research • Low levels of GA did not diminish vivipary in vp1 mutants. • This suggests that the GA and ABA signaling converges upstream from the site of vp1 action. • It was proposed that vp1 controls seed maturation and germination through 2 processes; 1. Transcriptional activator of ABA-inducible gene expression 2. ABA-independent repressor of germination specific gene expression
Uses in Bio-Tech • Causing seeds to germinate faster (skipping the dormancy stage of development) will results in plants growing to maturity faster. • This could result higher crop production.