Environmental Injury to Plants

290 Pages·1990·5.261 MB·English

by  Katterman, Frank (Eds.)

Environmental
Injury to Plants
EDITED BY
Frank Katterman
Department of Plant Sciences
College of Agriculture
University of Arizona
Tucson, Arizona
Academic Press, Inc.
Harcourt Brace Jovanovich, Publishers
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Copyright © 1990 by Academic Press, Inc.
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Library of Congress Cataloging-in-Publication Data
Environmental injury to plants / edited by Frank Katterman.
p. cm.
Papers from a one-day symposium held in June 1988 in Toronto,
Ont., sponsored by the American Chemical Society.
Includes bibliographical references.
ISBN 0-12-401350-3 (alk. paper)
1. Crops—Effect of stress on. 2. Plants, Effect of stress on.
3. Crops—Physiology. I. Katterman, Frank. II. American Chemical
Society.
SB112.5.E58 1990
632M-dc20 89-28741
CIP
Printed in the United States of America
90 91 92 93 9 8 7 6 5 4 3 2 1
Contributors
Numbers in parentheses indicate the pages on which the authors' contributions begin.
Hans J. Bohnert (173), Department Emmanuel Delhaize (231), CSIRO,
of Biochemistry, and Department of Division of Plant Research,
Molecular and Cellular Biology, Canberra, Australia
University of Arizona, Tucson,
Harold W. Gausman (257),
Arizona 85721
U. S. Department of Agriculture,
Agricultural Research Service,
Ray A. Bressan (137), Center for
Cropping Systems Research
Plant Environmental Stress
Laboratory, Lubbock, Texas 79401
Physiology, Department of
Horticulture, Purdue University, Charles Guy (35), Ornamental
West Lafayette, Indiana 47907 Horticulture Department, Institute
of Food and Agricultural Science,
Mark R. Brodl (113), Department of
University of Florida, Gainesville,
Biology, Knox College, Galesburg,
Florida 32611
Illinois 61401
Paul M. Hasegawa (137), Center for
Nicholas C. Carpita (137), Plant Environmental Stress
Department of Botany and Plant Physiology, Department of
Pathology, Purdue University, West Horticulture, Purdue University,
Lafayette, Indiana 47907 West Lafayette, Indiana 47907
Katrina Cornish (89), William J. Hurkman (205),
U. S. Department of Agriculture, U. S. Department of Agriculture,
Agricultural Research Service, Agriculture Research Service,
Western Regional Research Center, Western Regional Research Center,
Albany, California 94710 Albany, Californ1ia 94710
Nairn M. Iraki (137), Department
John C. Cushman (173), Department
of Botany and Plant Pathology,
of Biochemistry, University of
Purdue University, West Lafayette,
Arizona, Tiicson, Arizona 85721
Indiana 47907
E. Jay DeRocher (173), Department Paul J. Jackson (231), Genetics
of Molecular and Cellular Biology, Group, Life Sciences Divison, Los
University of Arizona, Tucson, Alamos National Laboratory, Los
Arizona 85721 Alamos, New Mexico 87544
Present address: Department of Botany, Hebrew University, Jerusalem, Israel.
IX
X Contributors
P. Christopher LaRosa (137), Center John W. Radin (89),
for Plant Environmental Stress U. S. Department of Agriculture,
Physiology, Department of Agricultural Research Service,
Horticulture, Purdue University, Western Cotton Research
West Lafayette, Indiana 47907 Laboratory, Phoenix, Arizona 85040
Ahmed Rayan (63), Department of
Daniel V. Lynch (17), Department of
Molecular and Cellular Biology,
Biology, Williams College,
University of Arizona, Tucson,
Williamstown, Massachusetts 01267
Arizona 85721
Nigel J. Robinson (231), Department
Kaoru Matsuda (63), Department of
of Biological Sciences, University of
Molecular and Cellular Biology, and
Durham Science Laboratories,
Department of Plant Sciences,
University of Arizona, Tucson, Durham DH1 3 LE, England
Arizona 85721
Narendra K. Singh (137),
Department of Botany and
Donald E. Nelson (137), Center for Microbiology, Auburn University,
Plant Environmental Stress Auburn, Alabama 36849
Physiology, Department of
Peter L. Steponkus (1), Department
Horticulture, Purdue University,
of Agronomy, Cornell University,
West Lafayette, Indiana 47907
Ithaca, New York 14853
Jerry E. Quisenberry (257), U.S. Pat J. Unkefer (231), Isotope and
Department of Agriculture, Structural Chemistry Group, Isotope
Agricultural Research Service, and Nuclear Chemistry Division,
Cropping Systems Research Los Alamos National Laboratory,
Laboratory, Lubbock, Texas 79401 Los Alamos, New Mexico 87545
Preface
The chapters in this book discuss various facets of plant environmental
stress that are of critical importance to those who are concerned with the
production of horticultural or agronomical plants on a large scale. Al­
though not all aspects of plant environmental stress have been included in
this publication, (for example, anerobiosis, pathogens, and pesticides) the
subjects covered are those of major concern to various commodity groups
in given regional sections of the United States. For example, in the north­
eastern, northern, Rocky Mountain, and midwest areas, freezing tempera­
tures are a major problem. As one moves toward the northwest, west, south
central, and southeast regions, chilling damage seems to be an additional
dominant factor. Finally, in the arid locations of the southwest, drought,
heat, and salt stress take their toll on economically important plants. Many
talented scientists are involved in the study of environmental plant stress.
This book is an outgrowth of a one-day symposium in Toronto that was
sponsored by the American Chemical Society in June of 1988 and represents
a sampling of these research workers.
The selection of topics should be of interest both to the scientific layman
and to the professional in a specialized subject area of plant stress. The
former, who may be a novice to the discipline as a whole, will be able to
obtain an overall idea (from the review nature of each chapter) of the recent
trends in each of the specific stress categories. On the other hand, the em­
phasis or bias for a particular trend will bring the professional up to date
in his or her particular area of interest.
The arrangement of subjects and chapters is as follows: The first three
chapters are concerned with both freezing and chill injury. P. L. Steponkus
uses a plant protoplast system to characterize the process of freezing injury
and cell lysis during an induced freeze/thaw cycle. D. V. Lynch examines
the role of membrane lipids in chilling injury and adds a new dimension to
one of the major tenents of the original membrane hypothesis. C. Guy fo­
cuses on the ability of the plant to increase its tolerance to freezing stress
through cold acclimation. He presents evidence and discusses the possibility
that a small number of genes control the physiological processes which lead
to a higher freezing tolerance of the plant cell.
Chapters 4 and 5 describe two different aspects of drought stress. K.
Matsuda and A. Rayan show that the reaction of plant tissue to water stress
depends upon both the physiological properties and the anatomical features
that regulate the transmission of the water deficit effect to the cells in ques-
xi
xii Preface
tion. K. Cornish and J. W. Radin review the role of abscisic acid (ABA) in
stomatal responses to drought stress. On the molecular level, evidence is
presented that ABA causes the appearance of new transcripts that nearly
match the set induced by drought stress.
Chapter 6 by M. R. Brodl represents a detailed review of heat shock
responses in plants during the past decade. Some of his work points to a po­
tential mechanism of induction for a heat shock response.
Chapters 7, 8, and 9 are involved with osmotic or salt stress. R. Bressan
and co-workers discuss salt tolerance on the cellular level. One of their sig­
nificant findings is a distinct difference in the occurrence of ionically bound
proteins to the walls of osmotically adapted and unadapted cells. J. C.
Cushman and co-workers, on the other hand, examine salt tolerance and
gene expression in the whole halophytic plant. They find an increase, a de­
crease, and a transient expression of several genes involved in the tolerance
reaction as a function of time. W. J. Hurkman reviews the use of two-di­
mensional gel electrophoresis to characterize the changes in gene expression
during salt stress. In addition, he describes the application of this tool for
his research on salt-tolerant barley.
Chapter 10 by P. J. Jackson et al. deals with the increasing presence of
heavy and toxic metals in the growing environment caused by the practice
of recycling sewage sludge into the soil for fertilizer. They discuss how
plants cope with this stress by means of a unique molecular adaptation.
Chapter 11 by H. W. Gausman and J. E. Quisenberry reviews the detec­
tion of plant stress by remote sensing devices. This technique can distinguish
between several kinds of environmental stress on plants in the field.
It will probably be apparent to the reader that most of the stress topics
discussed in this publication (e.g., osmotic, chill, drought, and heat) appear
to have a few of the induced proteins in common with one another. Future
research should further clarify a similar set of physiological or biomolecular
reactions or both, that are directly related to the respective shock protein
induction and to a development of tolerance for a given stress by the plant.
Frank R. Katterman
CHAPTER 1
Cold Acclimation and Freezing
Injury from a Perspective of the
Plasma Membrane
Peter L. Steponkus
Department of Agronomy
Cornell University
Ithaca, New York
I. Introduction v. Behavior of the Plasma Membrane
during Osmotic Excursions
II. The Freezing Process
VI. Effect of Severe Dehydration on the
III. Freeze-Induced Cell Dehydration Plasma Membrane
IV. The Role of the Plasma Membrane in VII. Summary
Intracellular Ice Formation
References
I. INTRODUCTION
Cold acclimation is a complex developmental process that occurs in winter
annuals, biennials, and perennials in which the ability to withstand freezing
temperatures increases during the fall and winter months. There is a wide
range in the increase in freezing tolerance that occurs, ranging from a few
degrees in herbaceous species to tens of degrees in winter cereals to over
100 degrees in some extremely hardy deciduous species. Because of the im­
pacts of freezing injury on a wide range of agricultural crop species, a con­
siderable amount of attention has been devoted to plant cold hardiness and
the process of cold acclimation.
During the cold-acclimation period, there is an orchestration of many
events that are required to achieve maximum cold hardiness. These events
include hormonal responses to environmental cues, altered gene activity and
new gene products, and alterations in metabolism resulting in the accumula­
tion of solutes and changes in lipid composition. Although seemingly dispa­
rate, these events ultimately contribute to the increased stability of cellular
membranes, including the plasma membrane. To understand the role of
Environmental Injury to Plants
1
Copyright © 1990 by Academic Press, Inc. All rights of reproduction in any form reserved.
2 Peter L. Steponkus
each facet, it is necessary to first understand the collective effect of these
changes on the primary site of freezing injury—the plasma membrane.
The plasma membrane is a primary site of freezing injury because of its
central role in cellular behavior during a freeze—thaw cycle. As the principal
barrier between the cytoplasm and the extracellular milieu, the semiperme­
able characteristics of the plasma membrane are of primary importance in
allowing for the efflux/influx of water during a freeze—thaw cycle while
restricting the efflux of intracellular solutes and, most important, preclud­
ing seeding of the cytosol by extracellular ice. Maintenance of these struc­
tural and functional characteristics during a freeze—thaw cycle is essential
to survival. There are an increasing number of reports on the effect of freez­
ing and cold acclimation on the plasma membrane because of its central
importance. Although there is a general consensus that the plasma mem­
brane is a primary site of freezing injury, there are divergent opinions on
the nature of injury, its cause, and the effect of cold acclimation. In part,
this is because different approaches have been taken to address these ques­
tions. Some of the studies have not dealt with the plasma membrane directly
and are only inferential because manifestations of injury are measured long
after the freeze—thaw event; other studies are more direct. Similarly, there
are many divergent reports regarding alterations in the plasma membrane
during cold acclimation.
To establish the nature and cause of injury during a freeze—thaw cycle,
we have based our approach on cryomicroscopic studies of isolated proto­
plasts. These studies, which describe the phenomenology of destabilization
of the plasma membrane during a freeze—thaw cycle, have been especially
useful in providing a perspective from which to view the molecular and
cellular aspects of both freezing injury and cold acclimation; they will be
reviewed in this chapter. These studies have focused on winter rye {Secale
céréale L. cv. Puma), which is among the most cold-hardy winter cereals.
Following cold acclimation under artificial conditions (5°C and 12-hr
daylength), the cold hardiness increases from —5 to — 25°C over a period
of 4 weeks. Protoplasts isolated from the leaves of the seedlings also reflect
this increase in hardiness, even though the conditions during the freeze—
thaw cycle are different from those experienced during freezing in situ.
II. THE FREEZING PROCESS
During cooling of a protoplast suspension, ice formation typically occurs
first in the aqueous suspending medium. Ice formation occurs either as a
result of heterogeneous nucleation or seeding by an ice crystal. During the
subsequent growth of the ice crystals, solutes and gases are largely excluded
1. Cold Acclimation and Freezing Injury 3
from the ice matrix and accumulate in an unfrozen portion of the partially
frozen mixture. During cooling to a given subzero temperature, ice forma­
tion will continue until the chemical potential of the unfrozen solution is in
equilibrium with the chemical potential of the ice, which is a direct function
of the subzero temperature. At equilibrium, the osmolality of the unfrozen
solution will be equal to (273 — T)/1.86. Thus, when a solution is cooled
and seeded at its freezing point, the osmolality of the unfrozen portion of
the solution increases linearly as a function of the subzero temperature (e.g.,
0.53 at -1°C, 2.69 at -5°C, 5.38 at -10°C, 10.75 at -20°C).
At any given subzero temperature, the osmolality of the unfrozen solu­
tion is independent of the initial osmolality of the solution (see Mazur,
1970). However, the proportion of the original solution that remains un­
frozen at any given subzero temperature depends on the initial osmolality
and the osmotic coefficient of the solute. The unfrozen portion is most accu­
rately determined from the liquidus curve of the phase diagram for the solu­
tion, with the fraction (weight percent) of the unfrozen solution calculated
as the ratio of the initial solute concentration (weight percent) to the solute
concentration (weight percent) in the unfrozen portion at a given subzero
temperature (see Rail et ai, 1983). For example, during freezing of a 0.53
osm sorbitol solution over the range of 0 to -20°C, approximately 28%
of the solution remains unfrozen at -5°C, 18% at -10°C, and 14% at
-20°C. If the initial osmolality of the solution is doubled to 1.06, the os­
molality of the unfrozen solution at any given subzero temperature will be
the same as the more dilute solution, but less solution will have to be frozen
before the unfrozen solution is sufficiently concentrated to achieve the equi­
librium osmolality (e.g., approximately 48% of the solution will remain
unfrozen at -5°C, 32% at -10°C, and 24% at -20°C).
III. FREEZE-INDUCED CELL DEHYDRATION
Because of the freeze-induced concentration of the suspending medium,
there will be a gradient in the chemical potential between the extracellular
solution and the intracellular solution. As a result, the protoplasts will re­
spond osmotically and will begin to dehydrate. The rate of water efflux will
be a function of the magnitude of the gradient in chemical potential between
the intracellular and the extracellular solution, the water permeability of
the plasma membrane, and the area to volume ratio of the cell. The extent
of dehydration will be a function of the external osmolality of the suspend­
ing medium, which is a direct function of the subzero temperature. At equi­
librium, the extent of cell dehydratio_n 1can be estimated from the Boyle van't
Hoff relationship V = V + x(osm ). Because of the extremely high solute
b
4 Peter L. Steponkus
concentrations that are effected during the freezing of aqueous solutions,
the extent of freeze-induced cell dehydration will be considerable. For ex­
ample, at — 5°C, the osmotic potential of the suspending medium is approx­
imately — 6 MPa and over 80% of the osmotically active water will be
removed from the protoplasts. At - 10°C, the osmotic potential is approxi­
mately — 12 MPa and more than 90% of the osmotically active water will
be removed. During warming of the suspension and melting of the suspend­
ing medium, the gradient in chemical potential will be reversed and, if the
plasma membrane has not been destabilized, the cells will expand osmoti­
cally. Thus, during a freeze—thaw cycle, the plasma membrane must remain
stable in the presence of extremely high solute concentrations and must be
able to withstand the mechanical stresses incurred during the large osmotic
excursions; otherwise survival of the cell is precluded. Accordingly, destabi-
lization of the plasma membrane can occur as a result of different stresses
in the cellular environment. In studies of protoplasts isolated from leaves
of rye (Secale céréale L. cv. Puma), the conditions that lead to destabiliza-
tion of the plasma membrane have been characterized for each of these
possibilities (see Steponkus, 1984; Steponkus and Lynch, 1989a).
IV. THE ROLE OF THE PLASMA MEMBRANE IN
INTRACELLULAR ICE FORMATION
Cell dehydration is only possible as long as ice formation does not occur in the
cytosol. Two conditions are required for intracellular ice formation: (1) the
cytosol must be supercooled, and (2) it must be either nucleated or seeded.
Both conditions are influenced by characteristics of the plasma membrane.
Supercooling of the cytosol will occur during cooling, with the extent of
supercooling a function of the rate of cooling (heat transfer) relative to the
efflux of water (mass transfer). Water flux will be determined by the water
permeability of the plasma membrane, the surface area to volume ratio of
the protoplast, and the magnitude of the gradient in chemical poten­
tial of the extracellular solution and the cytosol. For a given set of condi­
tions, the faster the rate of cooling, the greater the extent of supercooling.
However, although there is a strong cooling rate dependence for intracellu­
lar ice formation, the probability of intracellular ice formation is not a sim­
ple function of the extent of supercooling (Dowgert and Steponkus, 1983).
Instead, the probability of intracellular ice formation will increase only
when the cells are supercooled at temperatures below some characteristic
"ice nucleation temperature" (Mazur, 1970). A quantitative prediction of
the temperature and cooling rate dependence of intracellular ice formation
in isolated protoplasts requires information on the probability distribution