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Signaling interplay between PARP1 and ROS regulates stress-induced cell death and developmental changes in
Hina Mir1, Jyotika Rajawat1, Iqbal Vohra1
1Department of Biochemistry, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara, 390 002, Gujarat, India.
Experimental Cell Research
|November 14, 2020
Summary
Poly (ADP-ribose) polymerase-1 (PARP1) is a DNA damage sensor. This study reveals reactive oxygen species (ROS) significantly influence PARP1
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Poly (ADP-ribose) polymerase-1 (PARP1) functions as a crucial DNA damage sensor, regulating cellular repair and death pathways.
- Previous research established PARP1's role in Dictyostelium discoideum development and stress-induced cell death.
Purpose of the Study:
- To investigate the role of reactive oxygen species (ROS) in PARP1-mediated cellular responses under various stress conditions in D. discoideum.
- To elucidate the differential activation kinetics of PARP1 and the involvement of ROS in starvation and cadmium-induced cell death.
Main Methods:
- Monitoring PARP1 activation and Poly (ADP-ribose) accumulation under starvation and cadmium stress.
- Assessing the impact of ATP and NAD+ depletion on starvation-induced PARP1 activation.
- Evaluating the effects of cadmium dose and glutathione (GSH) on cell death and developmental arrest.
Main Results:
- Cadmium stress rapidly increased Poly (ADP-ribose) levels, while PARP1 activation was delayed.
- Starvation-induced PARP1 activation correlated with ATP/NAD+ depletion; PARP inhibition offered protection.
- Starvation triggered a biphasic cell death: an early ROS-driven necrotic phase and a later PARP1- and ROS-dependent paraptotic phase.
- Cadmium induced dose-dependent cell death (paraptosis at low dose, necrosis at high dose).
- Glutathione (GSH) rescued cells from cadmium-induced death and developmental arrest, restoring redox balance.
Conclusions:
- ROS play a critical role in modulating PARP1 activity and dictating cell fate under stress.
- PARP1-mediated cell death pathways are distinct under starvation and cadmium exposure.
- Restoring redox balance with GSH can counteract stress-induced developmental arrest and cell death in D. discoideum.
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