4.6 Review

Calcium Signaling in Plant Programmed Cell Death

Journal

CELLS
Volume 10, Issue 5, Pages -

Publisher

MDPI
DOI: 10.3390/cells10051089

Keywords

programmed cell death; calcium signal; hypersensitive response; abiotic stress; development; signal crosstalk

Categories

Funding

  1. Natural Science Foundation of Zhejiang Province [LY20C020001, LY18C020007]
  2. Science and Technology Development Plan of Hangzhou [20180432B10]
  3. China postdoctoral Science Foundation [2019M653803]

Ask authors/readers for more resources

Programmed cell death (PCD) in plants functions to maintain cellular homeostasis by eliminating old or damaged cells. Calcium signaling plays a crucial role in the induction of PCD, yet the specific mechanisms remain unclear.
Programmed cell death (PCD) is a process intended for the maintenance of cellular homeostasis by eliminating old, damaged, or unwanted cells. In plants, PCD takes place during developmental processes and in response to biotic and abiotic stresses. In contrast to the field of animal studies, PCD is not well understood in plants. Calcium (Ca2+) is a universal cell signaling entity and regulates numerous physiological activities across all the kingdoms of life. The cytosolic increase in Ca2+ is a prerequisite for the induction of PCD in plants. Although over the past years, we have witnessed significant progress in understanding the role of Ca2+ in the regulation of PCD, it is still unclear how the upstream stress perception leads to the Ca2+ elevation and how the signal is further propagated to result in the onset of PCD. In this review article, we discuss recent advancements in the field, and compare the role of Ca2+ signaling in PCD in biotic and abiotic stresses. Moreover, we discuss the upstream and downstream components of Ca2+ signaling and its crosstalk with other signaling pathways in PCD. The review is expected to provide new insights into the role of Ca2+ signaling in PCD and to identify gaps for future research efforts.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available