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A β-glucuronidase (GUS) Based Cell Death Assay
Published on: May 6, 2011
Endoplasmic reticulum stress-induced programmed cell death in soybean cells
Anna Zuppini1, Lorella Navazio, Paola Mariani
1Dipartimento di Biologia, Università di Padova, 35131 Padova, Italy. zuppini@civ.bio.unipd.it
Journal of Cell Science
|May 26, 2004
Summary
The endoplasmic reticulum plays a role in plant programmed cell death. Cyclopiazonic acid triggers cell death in soybean cells by inducing endoplasmic reticulum stress and mitochondrial signaling.
Area of Science:
- Plant Biology
- Cell Biology
- Biochemistry
Background:
- The endoplasmic reticulum (ER) is implicated in programmed cell death (PCD) in animal cells.
- Its role in plant PCD is less understood, prompting investigation into ER signaling pathways.
Purpose of the Study:
- To investigate the role of the endoplasmic reticulum in plant programmed cell death.
- To analyze the effects of cyclopiazonic acid (CPA), an ER Ca2+-pump blocker, on soybean cells.
Main Methods:
- Treatment of soybean cells with cyclopiazonic acid.
- Monitoring cytosolic Ca2+ concentration and ER stress.
- Assessing markers of programmed cell death, including H2O2 accumulation, cytochrome c release, caspase-like protease activation, and morphological changes.
- Using a Ca2+ chelator (BAPTA) to evaluate the role of Ca2+ in CPA-induced cell death.
Main Results:
- CPA induced ER stress and a biphasic increase in cytosolic Ca2+ in soybean cells.
- CPA triggered a cell death program characterized by H2O2 accumulation, cytochrome c release, and caspase-like protease activation.
- Chelation of cytosolic Ca2+ did not inhibit CPA-induced cell death, suggesting Ca2+ is not the sole mediator.
Conclusions:
- The endoplasmic reticulum is involved in regulating CPA-induced programmed cell death in soybean cells.
- Mitochondria also play a role, likely through cross-talk with the ER.
- This study provides evidence for ER-mitochondria communication in plant PCD.
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