SIP1, a novel SOS2 interaction protein, is involved in salt-stress tolerance in Arabidopsis
Copyright © 2018 Elsevier Masson SAS. All rights reserved.
Veröffentlicht in: | Plant physiology and biochemistry : PPB. - 1991. - 124(2018) vom: 30. März, Seite 167-174 |
---|---|
1. Verfasser: | |
Weitere Verfasser: | , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2018
|
Zugriff auf das übergeordnete Werk: | Plant physiology and biochemistry : PPB |
Schlagworte: | Journal Article Arabidopsis Protein interaction SIP1 SOS2 Salt stress Arabidopsis Proteins SOS2 protein, Arabidopsis EC 2.7.1.- Protein Serine-Threonine Kinases |
Zusammenfassung: | Copyright © 2018 Elsevier Masson SAS. All rights reserved. A novel salt overly-sensitive 2 (SOS2) interaction protein was identified by yeast two hybrid (Y2H) library and was referred to as SOS2 interaction protein 1 (SIP1). SIP1 belongs to a plant-specific protein family, which contains a conserved domain that corresponds to a putative N-acetyltransferase. The members of this family are tolerant to heavy metals and oxidative stress. Here, SIP1 was identified as a salt-responsive gene. The sos2×sip1-1 double mutant was more sensitive than the sos2 single mutant upon salt stress, whereas the overexpression of SIP1 gene enhanced the plant salt tolerance, suggesting that SIP1 was involved in plant salt tolerance. We also found that SIP1 increasingly accumulated in response to salt stress, and this accumulation was inhibited in the sos2 mutant background. This finding suggests that the function of SIP1 upon salt stress was dependent on SOS2 protein. Further investigation suggested that SIP1 improved Arabidopsis tolerance to salt stress by reducing the ROS accumulation. Taken together, these findings reveal a novel function of SIP1 in adjusting Arabidopsis adaptation to salt stress |
---|---|
Beschreibung: | Date Completed 12.07.2018 Date Revised 04.12.2021 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1873-2690 |
DOI: | 10.1016/j.plaphy.2018.01.018 |