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Revealing programmed cell death events during flower (petal) senescence

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Abstract Background Flower petals serve to attract pollinators and inherently have a short lifespan. The senescence of these plant parts is programmed in the developmental plan of the flower. Also at the cellular level, petal cell death is highly programmed, going through a number of phases that culminate in cellular suicide [programmed cell death (PCD)]. The signalling, biochemical, molecular and gene determinants involved in the regulation of PCD and the morphological characteristics of the process in flower petals have been described to some extent. Nonetheless, important issues of theoretical and practical significance related to PCD functioning and its contribution to petal deterioration remain unsolved. Scope In this review, we discuss the occurrence and role of PCD in petal senescence in models of ornamental plants. For comparison, the distinctive and common features of plant and animal types of PCD are outlined. The two major plant cell death categories [vacuolar (V) PCD, reminiscent of animal autophagic PCD, and apoptosis-like (AL) PCD, sharing features with animal apoptosis] and their contribution to petal senescence are discussed. Conclusions The findings indicate that cellular PCD is tightly connected to petal senescence and support the view that senescence is a specific form of developmental PCD (senescence/PCD), dominated by large-scale autophagy and eventual breakdown of the vacuolar membrane. Depending on the measured PCD markers, petal cell death is often characterized as being either V-PCD or AL-PCD. However, alongside the ongoing V-PCD, in early or late stages of senescence, often AL-PCD-associated features are observed. This indicates that, in senescing petal cells, both PCD pathways operate in parallel and are, presumably, interconnected. The specific conditions might determine their relative contributions to cell death. The cell death cascade might, in general, start earlier in parenchyma than in epidermal cells. In a fully open, visibly non-senescent flower, a large part of the mesophyll cells may already have died or even disappeared, indicating that petal senescence is well on its way and cannot be reversed. Petal abscission can occur in both non-senescent and senescent petals, and its regulation seems independent from petal PCD.
Title: Revealing programmed cell death events during flower (petal) senescence
Description:
Abstract Background Flower petals serve to attract pollinators and inherently have a short lifespan.
The senescence of these plant parts is programmed in the developmental plan of the flower.
Also at the cellular level, petal cell death is highly programmed, going through a number of phases that culminate in cellular suicide [programmed cell death (PCD)].
The signalling, biochemical, molecular and gene determinants involved in the regulation of PCD and the morphological characteristics of the process in flower petals have been described to some extent.
Nonetheless, important issues of theoretical and practical significance related to PCD functioning and its contribution to petal deterioration remain unsolved.
Scope In this review, we discuss the occurrence and role of PCD in petal senescence in models of ornamental plants.
For comparison, the distinctive and common features of plant and animal types of PCD are outlined.
The two major plant cell death categories [vacuolar (V) PCD, reminiscent of animal autophagic PCD, and apoptosis-like (AL) PCD, sharing features with animal apoptosis] and their contribution to petal senescence are discussed.
Conclusions The findings indicate that cellular PCD is tightly connected to petal senescence and support the view that senescence is a specific form of developmental PCD (senescence/PCD), dominated by large-scale autophagy and eventual breakdown of the vacuolar membrane.
Depending on the measured PCD markers, petal cell death is often characterized as being either V-PCD or AL-PCD.
However, alongside the ongoing V-PCD, in early or late stages of senescence, often AL-PCD-associated features are observed.
This indicates that, in senescing petal cells, both PCD pathways operate in parallel and are, presumably, interconnected.
The specific conditions might determine their relative contributions to cell death.
The cell death cascade might, in general, start earlier in parenchyma than in epidermal cells.
In a fully open, visibly non-senescent flower, a large part of the mesophyll cells may already have died or even disappeared, indicating that petal senescence is well on its way and cannot be reversed.
Petal abscission can occur in both non-senescent and senescent petals, and its regulation seems independent from petal PCD.

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