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.
Highlights
The COP9 signalosome (CSN) is an evolutionarily conserved multiprotein complex comprised of eight subunits (CSN1 to CSN8) [1]
We employed viable hypomorphic csn mutants to study the role of CSN in response to abiotic stress. While these mutants are hypersensitive to salinity and UV-C, growth of csn5a-1 was enhanced after heat stress
After 2 days of cold stratification (4 ◦ C in dark) plates were transferred to the growth chamber at 21 ◦ C under long day condition (16 h white light at 100 μmol m2 s−1 and 8 h darkness) at 70% relative humidity; 10 days after sowing (DAS), seedlings were transferred to the soil, and stress treatment was given at 14 DAS
Summary
The COP9 (constitutive photomorphogenesis 9) signalosome (CSN) is an evolutionarily conserved multiprotein complex comprised of eight subunits (CSN1 to CSN8) [1]. Complete loss of any subunit results in pleiotropic constitutively photomorphogenic/de-etolated/fusca (cop/det/fus) phenotype with characteristic stunted growth, open cotyledons in dark-grown seedling, short hypocotyl, and anthocyanin pigment accumulation [3,4]. The CSN regulates a number of hormonal signaling pathways through its action as a deneddylase regulating ubiquitin-mediated protein stability [5]. CSN regulates responses to auxin, jasmonate, and gibberellic acid, as well as flower development, through its regulation of Cullin-RING ubiquitin E3 ligases (CRLs) such as the SKP1, Cullin and F-box-containing. The CSN regulates other CRLs such as those containing CUL3 (cullin 3) and CUL4 [11,12]
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