Within the extreme diversity of aquatic and terrestrial plant genera, each has characteristic cell wall forms. A number of hypotheses have been advanced to explain differences in microfibril arrangements across anyone such wall. Of those, only the 'multinet' theory, which involves the postulation of reorientation of microfibrils caused by cell extension, now has a substantial number of ad herents. However, many scientists are sceptical of its validity; obviously it is incompatible with various observed microfibril arrangements. The tenet of this study is that any such hypothesis can be valid…mehr
Within the extreme diversity of aquatic and terrestrial plant genera, each has characteristic cell wall forms. A number of hypotheses have been advanced to explain differences in microfibril arrangements across anyone such wall. Of those, only the 'multinet' theory, which involves the postulation of reorientation of microfibrils caused by cell extension, now has a substantial number of ad herents. However, many scientists are sceptical of its validity; obviously it is incompatible with various observed microfibril arrangements. The tenet of this study is that any such hypothesis can be valid only if it is applicable to all plant forms and wall types. Initially, reanalyses are made of data claimed to confirm justification for multi net postulations. The results show that previous deductions from those data, in support of multinet, are subject to serious challenge. Similarly, a re-examination of the observations, which inspired the multinet theory, shows they have a more logical explanation. Herein, it is concluded that cell wall development involves biophysical factors, which neces sarily prevent multinet's postulated large reorientations of microfibrils, after their formation. Unfortunately the previously most recent published theory, which is based on the absence of reorientation during extension, fails to answer the fundamental question of how alternating orientations between lamellae are controlled, or explain variations in thickness of wall layers. Extensive published data are used to identify forces involved in cell wall development.Hinweis: Dieser Artikel kann nur an eine deutsche Lieferadresse ausgeliefert werden.
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Inhaltsangabe
I. Introduction.- II. Reassessment of data relating to the multinet theory of microfibril reorientation.- 1. Data obtained by Probine and Preston (1961) and Green and Chapman (1955).- 2. Data obtained by Frei and Preston (1961a, b).- 3. Data obtained by Green (1960a).- 4. Data obtained by Gertel and Green (1977).- 5. Recent observations claimed to support MGH.- III. Significance of biophysics and genetics in primary growth.- 1. Biophysical interaction with microfibril arrangement in the meristematic area.- 2. Genetic influence on orientations of microfibril additions during extension growth.- IV. Reassessment of data on tip growth and conclusions on MGH.- 1. Reorientation of microfibrils during tip growth.- 2. Conclusions on the multinet hypothesis and reorientation possibilities.- V. Wide variety of microfibril arrangements in plant cell walls.- VI. Critical preliminary considerations for a new theory on microfibril orientation.- 1. Fundamental requirements.- 2. Indicators of the importance of physical factors.- 3. Physical interactions between microfibrils and matrix materials.- 4. Effect of bonding of microfibrils and stress direction on cell wall stiffness and orientation of microfibrils.- 5. Stress distribution effects through the cell wall thickness.- 6. Relationship between helical orientation and the direction of cell extension.- VII. Biophysics of orientation of microfibrils in surface growth.- 1. Identification of the fundamental control factors.- 2. Induction of helical orientation in extension growth.- 3. Reduction of initial helical angle with reducing extension rate.- 4. Operation of critical structural controls in tubular cells with one dominant helical orientation of microfibrils.- 5. Biophysical considerations in the optimum use of plant energy.- 6. Orientation interaction with experimental limitation on strain.- 7. Spiral growth induced by the helical orientation of microfibrils.- 8. Effects of extension growth on the variability of orientation within microfibrils.- 9. The nature and significance of axial striations in Nitella internodal cells.- 10. Formation of branches and development of characteristic orientation of microfibrils.- 11. General nature of lamellae development and induced reactions.- 12. Controls for microfibril orientation changes between lamellae.- 13. Biophysical influence in thickening walls of epidermal and collenchyma cells.- 14. Biophysics of corner thickenings in collenchyma cells.- 15. Association of axial rib thickenings and prominent regular pit fields in parenchyma.- VIII. Helicoidal structure and comparable texture variations.- 1. Helicoidal structure.- 2. Herringbone texture.- 3. Problems in classifying texture as helicoidal, or herringbone, or other type.- 4. Classification of textures of particular plant tissues.- 5. Provisional general conclusions on cell wall texture.- IX. Biophysics of cell wall architecture in secondary wall formation.- 1. Preliminary considerations.- 2. Microfibril organization in the S2 wall layer.- 3. Microfibril organization in the S1 wall layer.- 4. Microfibril organization in the S3 wall layer.- 5. Alternating helical directions between S1, S2 and S3.- 6. Absence of an S3 layer in reaction wood and phloem fibres.- X. Biophysical basis for wall layer nomenclature.- XI. General discussion of the significance of biophysics in plant morphology.- XII. Literature cited.- List of appendices.- Appendix I Reorientation possible prior to microfibrils being fractured by overstrain.- Appendix II Possible reorientation of microfibril fragments.- 1. Effect of extension growth on orientation of microfibril fragments.- 2. The effect of spiral growth on reorientation of microfibril fragments.- Appendix III Hypothetical mean orientation of microfibrils resulting from extension growth in accordance with the multinet growth hypothesis.- 1. General assumptions.- 2. Results.- Appendix IV Interpretation of Green's (1960a) data on passive reorientation of microfibrils.- 1. Assumption of constant proportional crystallinity through the wall thickness.- 2. Green's extrapolation of curves.- 3. Curve slopes near outside face of wall.- 4. Microfibril orientation indicated by micrograph of polarized light effects..- Appendix V Alternative models for extension of cell walls.- 1. The isotropic cylinder model.- 2. The helical spring model.- 3. Comparison of isotropic cylinder and helical spring models.- Appendix VI Strain stimulation for microfibril orientation in epidermal cells.
I. Introduction.- II. Reassessment of data relating to the multinet theory of microfibril reorientation.- 1. Data obtained by Probine and Preston (1961) and Green and Chapman (1955).- 2. Data obtained by Frei and Preston (1961a, b).- 3. Data obtained by Green (1960a).- 4. Data obtained by Gertel and Green (1977).- 5. Recent observations claimed to support MGH.- III. Significance of biophysics and genetics in primary growth.- 1. Biophysical interaction with microfibril arrangement in the meristematic area.- 2. Genetic influence on orientations of microfibril additions during extension growth.- IV. Reassessment of data on tip growth and conclusions on MGH.- 1. Reorientation of microfibrils during tip growth.- 2. Conclusions on the multinet hypothesis and reorientation possibilities.- V. Wide variety of microfibril arrangements in plant cell walls.- VI. Critical preliminary considerations for a new theory on microfibril orientation.- 1. Fundamental requirements.- 2. Indicators of the importance of physical factors.- 3. Physical interactions between microfibrils and matrix materials.- 4. Effect of bonding of microfibrils and stress direction on cell wall stiffness and orientation of microfibrils.- 5. Stress distribution effects through the cell wall thickness.- 6. Relationship between helical orientation and the direction of cell extension.- VII. Biophysics of orientation of microfibrils in surface growth.- 1. Identification of the fundamental control factors.- 2. Induction of helical orientation in extension growth.- 3. Reduction of initial helical angle with reducing extension rate.- 4. Operation of critical structural controls in tubular cells with one dominant helical orientation of microfibrils.- 5. Biophysical considerations in the optimum use of plant energy.- 6. Orientation interaction with experimental limitation on strain.- 7. Spiral growth induced by the helical orientation of microfibrils.- 8. Effects of extension growth on the variability of orientation within microfibrils.- 9. The nature and significance of axial striations in Nitella internodal cells.- 10. Formation of branches and development of characteristic orientation of microfibrils.- 11. General nature of lamellae development and induced reactions.- 12. Controls for microfibril orientation changes between lamellae.- 13. Biophysical influence in thickening walls of epidermal and collenchyma cells.- 14. Biophysics of corner thickenings in collenchyma cells.- 15. Association of axial rib thickenings and prominent regular pit fields in parenchyma.- VIII. Helicoidal structure and comparable texture variations.- 1. Helicoidal structure.- 2. Herringbone texture.- 3. Problems in classifying texture as helicoidal, or herringbone, or other type.- 4. Classification of textures of particular plant tissues.- 5. Provisional general conclusions on cell wall texture.- IX. Biophysics of cell wall architecture in secondary wall formation.- 1. Preliminary considerations.- 2. Microfibril organization in the S2 wall layer.- 3. Microfibril organization in the S1 wall layer.- 4. Microfibril organization in the S3 wall layer.- 5. Alternating helical directions between S1, S2 and S3.- 6. Absence of an S3 layer in reaction wood and phloem fibres.- X. Biophysical basis for wall layer nomenclature.- XI. General discussion of the significance of biophysics in plant morphology.- XII. Literature cited.- List of appendices.- Appendix I Reorientation possible prior to microfibrils being fractured by overstrain.- Appendix II Possible reorientation of microfibril fragments.- 1. Effect of extension growth on orientation of microfibril fragments.- 2. The effect of spiral growth on reorientation of microfibril fragments.- Appendix III Hypothetical mean orientation of microfibrils resulting from extension growth in accordance with the multinet growth hypothesis.- 1. General assumptions.- 2. Results.- Appendix IV Interpretation of Green's (1960a) data on passive reorientation of microfibrils.- 1. Assumption of constant proportional crystallinity through the wall thickness.- 2. Green's extrapolation of curves.- 3. Curve slopes near outside face of wall.- 4. Microfibril orientation indicated by micrograph of polarized light effects..- Appendix V Alternative models for extension of cell walls.- 1. The isotropic cylinder model.- 2. The helical spring model.- 3. Comparison of isotropic cylinder and helical spring models.- Appendix VI Strain stimulation for microfibril orientation in epidermal cells.
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