Dataset Information

Cutting Out the Gaps Between Proteases and Programmed Cell Death.

ABSTRACT: To date, many animal models for programmed cell death (PCD) have been extensively characterized and classified while such efforts in plant types of PCD still remain poorly understood. However, despite a wide range of functional differences between PCD types in animals and plants, it is certain that all of them are regulated through the recruitment of proteases. Most importantly, proteases are able to perform proteolysis that results in a gain or loss of protein function. This principle relies on the presence of proteolytic cascades where proteases are activated upon various upstream stimuli and which lead to repetitive cell death. While protease activation, proteolytic cascades and targeted substrates are described in detail mainly for nematode, human, and mice models of apoptosis, for plants, only fragmentary knowledge of protease involvement in PCD exists. However, recently, data on the regulation of general plant PCD and protease involvement have emerged which deepens our understanding of the molecular mechanisms responsible for PCD in plants. With this in mind, this article highlights major aspects of protease involvement in the execution of PCD in both animals and plants, addresses obstacles and advances in the field and proposes recommendations for further research of plant PCD.

SUBMITTER: Balakireva AV

PROVIDER: S-EPMC6558192 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Cutting Out the Gaps Between Proteases and Programmed Cell Death.

Balakireva Anastasia V AV Zamyatnin Andrey A AA

Frontiers in plant science 20190604

To date, many animal models for programmed cell death (PCD) have been extensively characterized and classified while such efforts in plant types of PCD still remain poorly understood. However, despite a wide range of functional differences between PCD types in animals and plants, it is certain that all of them are regulated through the recruitment of proteases. Most importantly, proteases are able to perform proteolysis that results in a gain or loss of protein function. This principle relies on ...[more]

PMID: 31214222

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Project description:BackgroundVertebrate genomes undergo epigenetic reprogramming during development and disease. Emerging evidence suggests that DNA methylation plays a key role in cell fate determination in the retina. Despite extensive studies of the programmed cell death that occurs during retinal development and degeneration, little is known about how DNA methylation might regulate neuronal cell death in the retina.MethodsThe developing chicken retina and the rd1 and rhodopsin-GFP mouse models of retinal degeneration were used to investigate programmed cell death during retinal development and degeneration. Changes in DNA methylation were determined by immunohistochemistry using antibodies against 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC).ResultsPunctate patterns of hypermethylation paralleled patterns of caspase3-dependent apoptotic cell death previously reported to occur during development in the chicken retina. Degenerating rd1 mouse retinas, at time points corresponding to the peak of rod cell death, showed elevated signals for 5mC and 5hmC in photoreceptors throughout the retina, with the most intense staining observed in the peripheral retina. Hypermethylation of photoreceptors in rd1 mice was associated with TUNEL and PAR staining and appeared to be cCaspase3-independent. After peak rod degeneration, during the period of cone death, occasional hypermethylation was observed in the outer nuclear layer.ConclusionThe finding that cell-specific increases of 5mC and 5hmC immunostaining are associated with the death of retinal neurons during both development and degeneration suggests that changes in DNA methylation may play a role in modulating gene expression during the process of retinal degeneration. During retinal development, hypermethylation of retinal neurons associates with classical caspase-dependent apoptosis as well as caspase-3 independent cell death, while hypermethylation in the rd1 mouse photoreceptors is primarily associated with caspase-3 independent programmed cell death. These findings suggest a previously unrecognized role for epigenetic mechanisms in the onset and/or progression of programed cell death in the retina.

Dataset Information

Cutting Out the Gaps Between Proteases and Programmed Cell Death.

Publications

Cutting Out the Gaps Between Proteases and Programmed Cell Death.

Similar Datasets

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