CSN5A subunit of COP9 signalosome temporally buffers response to heat in arabidopsis

Amit Kumar Singh, Brijesh Singh Yadav, Shanmuhapreya Dhanapal, Mark Berliner, Alin Finkelshtein, Daniel A. Chamovitz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

The COP9 (constitutive photomorphogenesis 9) signalosome (CSN) is an evolutionarily conserved protein complex which regulates various growth and developmental processes. However, the role of CSN during environmental stress is largely unknown. Using Arabidopsis as model organism, we used CSN hypomorphic mutants to study the role of the CSN in plant responses to environmental stress and found that heat stress specifically enhanced the growth of csn5a-1 but not the growth of other hypomorphic photomorphogenesis mutants tested. Following heat stress, csn5a-1 exhibits an increase in cell size, ploidy, photosynthetic activity, and number of lateral roots and an upregulation of genes connected to the auxin response. Immunoblot analysis revealed an increase in deneddylation of CUL1 but not CUL3 following heat stress in csn5a-1, implicating improved CUL1 activity as a basis for the improved growth of csn5a-1 following heat stress. Studies using DR5::N7-VENUS and DII-VENUS reporter constructs confirm that the heat-induced growth is due to an increase in auxin signaling. Our results indicate that CSN5A has a specific role in deneddylation of CUL1 and that CSN5A is required for the recovery of AUX/IAA repressor levels following recurrent heat stress to regulate auxin homeostasis in Arabidopsis.

Original languageEnglish
Article number805
JournalBiomolecules
Volume9
Issue number12
DOIs
StatePublished - 2019

Funding

FundersFunder number
Guilia Meshulam
Israeli Centers for Research Excellence Program of the Planning and Budgeting Committee, Israel Science Foundation757/12
Israel Science Foundation060411552/18

    Keywords

    • Auxin signaling
    • COP9 signalosome
    • Cullin deneddylation
    • Hypomorphic mutants
    • VENUS reporter construct

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