Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.481169
Title: Developmental and molecular aspects of turion formation in Spirodela polyrrhiza and its induction by abscisic acid
Author: Smart, Cheryl Christine
ISNI:       0000 0001 3417 4410
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1982
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Abstract:
The ability of S. polyrrhiza to form turions in response to ABA, made it an ideal model for an investigation into the development of the dormant state and its regulation by ABA. Addition of ABA to a culture of S. polyrrhiza resulted in growth inhibition at concentrations as low as 10⁻⁹M, growth being completely arrested at 10⁻⁵M. However, over a single order of magnitude range around 10⁻⁷M, ABA also induced the production of turions. The morphological changes and structure of the vegetative frond and turion were characterised at both the light and electron microscope level, and the cellular differences between frond and turion cells investigated by detailed stereological analysis. It was found that only primordia ≤0.7 mm long could be induced by ABA to develop into turions. During the development of a cell, it acquires ABA sensitivity for turion formation, and is only in this state for approximately 14 hours. Ultrastructural analysis showed that the cells within this sensitivity window are still actively dividing, and the developmental switch -over to rapid cell expansion and separation is believed to mark the end of the cell's sensitivity to ABA. The turion of S. polyrrhiza is characterised by its small size, reniform shape and dark brown colouration. The mesophyll is undifferentiated and totally lacking the substantial aerenchyma development found in the vegetative frond. The cells of the turion, while reaching approximately the same final size as the vegetative frond cells, accumulate numerous starch grains, thick cell walls and large deposits of tannins and anthocyanin pigment, at the expense of vacuolar expansion. A comprehensive examination and evaluation of the biochemical parameters associated with turion formation was carried out. The developmental process leading to the formation of turions was accompanied by a repression of nucleic acid and protein synthesis and an enhancement of secondary metabolism. DNA synthesis in the developing turion was inhibited within 3 hours of ABA addition, followed by a repression of protein(especially soluble protein) synthesis after 24 hours, while RNA synthesis was not inhibited until 3 days. The inhibitory effect of ABA on protein synthesis was found to be selective and the synthesis of several novel proteins appeared to be induced. The relationship between the changes in the polypeptide and mRNA profiles during the development of the turion was investigated. The rapid general inhibition of protein synthesis at early stages of turion formation could not be accounted for by the levels of translatable mRNA, indicating an effect of ABA at the translational level. The specific alteration to the pattern of in vivo labelled proteins could however have resulted from control of the level of specific mRNAs for those particular proteins. Only after 3 days in aA, when the developing primordium is committed to the turion developmental pathway, is there a total inhibition in the production of mRNA leading to the shut -down of all primary processes and the onset of the irreversible events leading to the dormant state. No obvious ion effects causal to turion formation or initiation could be detected by compartmental analysis, although the ionic fluxes and concentrations of the mature turion were very different to those of the vegetative frond. Thus it was concluded that the mechanism of action of ABA in responsive tissue is the regulation of gene expression and the production of specific mRNAs; followed by a sequence of steps leading to inhibition of DNA, protein and RNA synthesis, inhibition of cell division, expansion and differentiation, and an enhancement of secondary metabolism. The molecular basis of the differential sensitivity to ABA which was found throughout this work is discussed in terms of receptor mechanisms.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.481169  DOI: Not available
Keywords: Genetics
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