The hormonal control of cell wall properties

A technique has been developed for the separation of auxin action and cell elongation. Avena coleoptile sections are treated with auxin under conditions of nonexpansion. This is followed by expansion of the sections in water containing an inhibitor which blocks all auxin action. Under aerobic condit...

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Main Author: Cleland, Robert Erskine
Format: Others
Published: 1957
Online Access:https://thesis.library.caltech.edu/2795/1/Cleland_re_1957.pdf
Cleland, Robert Erskine (1957) The hormonal control of cell wall properties. Dissertation (Ph.D.), California Institute of Technology. doi:10.7907/2PSQ-9548. https://resolver.caltech.edu/CaltechETD:etd-07012004-102944 <https://resolver.caltech.edu/CaltechETD:etd-07012004-102944>
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spelling ndltd-CALTECH-oai-thesis.library.caltech.edu-27952019-12-22T03:07:31Z The hormonal control of cell wall properties Cleland, Robert Erskine A technique has been developed for the separation of auxin action and cell elongation. Avena coleoptile sections are treated with auxin under conditions of nonexpansion. This is followed by expansion of the sections in water containing an inhibitor which blocks all auxin action. Under aerobic conditions, auxin initiates a loosening of the cell wall. The loosening can then persist over short periods of non-expansion under anaerobic conditions. The loosening can be abolished by general metabolic inhibitors such as KCN or counteracted by an auxin-independent stiffening process. The loosening is due to an increase in the plasticity of the cell wall. Ethionine administered during either phase of the process inhibits the residual auxin effect, suggesting that transmethylation is involved in the increase in plasticity. The metabolism of the cell wall components has been investigated by the use of labeled glucose and labeled methionine. The only effect of auxin which was found was an increased rate of incorporation of label from both glucose and methionine into the methyl ester groups of pectin. This increase is abolished by the same inhibitors which abolish the auxin-induced cell wall loosening. It is proposed that the increase in rate of pectin methyl ester incorporation is an integral part of the cell wall loosening process. Incorporation of label from methionine C-14 into the pectin fraction has also been achieved with homogenates of Avena coleoptile sections although the rate is markedly decreased by homogenization. A procedure has been developed for obtaining reproducible results with such homogenates. Dialysis of the homogenate supernatant after solubilization of the pectin by boiling has proven satisfactory. About 85 percent of the label from methionine C-14 incorporated into the pectin of intact tissues is in the form of esterified methyl groups. Upon homogenization of the tissues, however, only 20 percent of the label is located in the methyl groups. 1957 Thesis NonPeerReviewed application/pdf https://thesis.library.caltech.edu/2795/1/Cleland_re_1957.pdf https://resolver.caltech.edu/CaltechETD:etd-07012004-102944 Cleland, Robert Erskine (1957) The hormonal control of cell wall properties. Dissertation (Ph.D.), California Institute of Technology. doi:10.7907/2PSQ-9548. https://resolver.caltech.edu/CaltechETD:etd-07012004-102944 <https://resolver.caltech.edu/CaltechETD:etd-07012004-102944> https://thesis.library.caltech.edu/2795/
collection NDLTD
format Others
sources NDLTD
description A technique has been developed for the separation of auxin action and cell elongation. Avena coleoptile sections are treated with auxin under conditions of nonexpansion. This is followed by expansion of the sections in water containing an inhibitor which blocks all auxin action. Under aerobic conditions, auxin initiates a loosening of the cell wall. The loosening can then persist over short periods of non-expansion under anaerobic conditions. The loosening can be abolished by general metabolic inhibitors such as KCN or counteracted by an auxin-independent stiffening process. The loosening is due to an increase in the plasticity of the cell wall. Ethionine administered during either phase of the process inhibits the residual auxin effect, suggesting that transmethylation is involved in the increase in plasticity. The metabolism of the cell wall components has been investigated by the use of labeled glucose and labeled methionine. The only effect of auxin which was found was an increased rate of incorporation of label from both glucose and methionine into the methyl ester groups of pectin. This increase is abolished by the same inhibitors which abolish the auxin-induced cell wall loosening. It is proposed that the increase in rate of pectin methyl ester incorporation is an integral part of the cell wall loosening process. Incorporation of label from methionine C-14 into the pectin fraction has also been achieved with homogenates of Avena coleoptile sections although the rate is markedly decreased by homogenization. A procedure has been developed for obtaining reproducible results with such homogenates. Dialysis of the homogenate supernatant after solubilization of the pectin by boiling has proven satisfactory. About 85 percent of the label from methionine C-14 incorporated into the pectin of intact tissues is in the form of esterified methyl groups. Upon homogenization of the tissues, however, only 20 percent of the label is located in the methyl groups.
author Cleland, Robert Erskine
spellingShingle Cleland, Robert Erskine
The hormonal control of cell wall properties
author_facet Cleland, Robert Erskine
author_sort Cleland, Robert Erskine
title The hormonal control of cell wall properties
title_short The hormonal control of cell wall properties
title_full The hormonal control of cell wall properties
title_fullStr The hormonal control of cell wall properties
title_full_unstemmed The hormonal control of cell wall properties
title_sort hormonal control of cell wall properties
publishDate 1957
url https://thesis.library.caltech.edu/2795/1/Cleland_re_1957.pdf
Cleland, Robert Erskine (1957) The hormonal control of cell wall properties. Dissertation (Ph.D.), California Institute of Technology. doi:10.7907/2PSQ-9548. https://resolver.caltech.edu/CaltechETD:etd-07012004-102944 <https://resolver.caltech.edu/CaltechETD:etd-07012004-102944>
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