Programmed Cell Death as a Response to High Light, UV and Drought Stress in Plants - Abiotic Stress: Plant Responses and Applications in Agriculture - page 208

female or male within a bisexual fl oral meristem [3]. The production of complex leaf shapes
also frequently employs PCD. Such remodeling of leaf blades occurs in Monstera obliqua ,
Monstera deliciosa or lace plant [4]. These species tend to induce death pathway in some
patches of cells and thus form distinctive perforations within the leaf [5]. PCD is also engag‐
ed in such processes as dying of aleurone cells in seeds of monocots, root cap shedding or
anther dehiscence. Senescence, which is the final stage of vegetative and generative develop‐
ment, preceding plant organs death, also involves PCD. In deciduous trees, senescence is ex‐
hibited in the changes of leaves color developing during autumn. It enables the active
turnover of cellular material and its use in other organs. For example, nutrients, such as ni‐
trogen, recycled from leaves are used for the synthesis of proteins that will be stored in
stems and will support growth in the following vegetative season. Moreover, PCD during
senescence helps to block spreading of diseases to still vital parts of the plant [6].
Developmental PCD is induced by internal factors and occurs at defined time and in partic‐
ular plant tissue. On the contrary, environmentally-induced PCD is triggered by different
stimuli ranging from pathogen infection to environmental factors [7]. During infection of
plant leaves by pathogens, a specific gene-for-gene (avr-R) interaction triggers defense re‐
sponses. Upon such plant-microbe interaction, cell death takes a form of so-called hypersen‐
sitive response (HR) and includes a burst of reactive oxygen species (ROS). HR leads to the
formation of a lesion which is clearly delimited from surrounding healthy cells and thus
prevents the spread of pathogen throughout the plant tissue. Certain mutations in many
plant species have been demonstrated to cause spontaneous, HR-resembling lesions, which
suggests that this type of cell death is under a genetic control. Such lesion mimic mutants
are divided into two groups: related to the initiation of PCD (inappropriate induction of
PCD and formation of localized lesion spots) or propagation (inability to stop PCD once it
has been initiated). Both these groups of mutants are currently widely investigated since
they can provide insight into the general mechanism of PCD in plants [8-12]. The existence
of these two classes suggests that genetically distinct processes underlie the lesion forma‐
tion: the initiation of cell death and its spread to surrounding cells as well as the existence of
communication signals between dying and healthy cells in determining the lesion size.
In natural habitats, plants are constantly exposed to a variety of environmental stresses that
can lead to the disturbance in cellular homeostasis and consequently limit crop yield. Pro‐
grammed cell death is a fundamental cellular process associated with the defense responses
to abiotic stimuli such as excessive irradiation, ozone, ultraviolet radiation, heat, cold,
drought or flooding. One of the example factor triggering PCD is hypoxia, a condition in
which plant is deprived of oxygen supply. In response to waterlogging and lower O 2 con‐
centration in the ground, cortex of the root can form aerating tissue called aerenchyma [13].
The internal air spaces are generated through PCD and facilitate gas diffusion from aerial
organs to waterlogged roots [14]. Although it is unfavorable for biomass production, the se‐
lective death of cells and tissues under abiotic stresses eventually provides survival advan‐
tages for the whole organism. At the organismal level, PCD helps to maintain tissue and
organ homeostasis, enables developmental adaptation and nutrient resorption from dying
cells thus increases the probability of survival. It also leads to the signals transduction from