Disease relevance of LSD1

• These treatments included inoculation with virulent and avirulent Pseudomonas syringae strains, spontaneous lesion formation in the lsd1 mutant, and treatment with the salicylic acid (SA) analogs INA (2,6-dichloroisonicotinic acid) and BTH (benzothiadiazole) [1].

High impact information on LSD1

• A novel zinc finger protein is encoded by the Arabidopsis LSD1 gene and functions as a negative regulator of plant cell death [2].
• LSD1 is constitutively expressed, consistent with the mutant phenotype [2].
• These domains are present in three additional Arabidopsis genes, suggesting that LSD1 defines a zinc finger protein subclass [2].
• Surprisingly, AtbZIP10 can be retained outside the nucleus by LSD1, a protein that protects Arabidopsis cells from death in the face of oxidative stress signals [3].
• The disease resistance signaling components EDS1 and PAD4 are essential regulators of the cell death pathway controlled by LSD1 in Arabidopsis [4].

Biological context of LSD1

• Thus, LSD1 monitors a superoxide-dependent signal and negatively regulates a plant cell death pathway [2].
• The predicted LSD1 protein contains three zinc finger domains, defined by CxxCxRxxLMYxxGASxVxCxxC [2].
• We propose that the roles of LSD1 in light acclimation and in restricting pathogen-induced cell death are functionally linked [5].
• These vectors were used to investigate and visualize homodimerization of the basic leucine zipper (bZIP) transcription factor bZIP63 and the zinc finger protein lesion simulating disease 1 (LSD1) from Arabidopsis as well as the dimer formation of the tobacco 14-3-3 protein T14-3c [6].
• LSD1 likely functions as a cellular hub, where its interaction with AtbZIP10 and additional, as yet unidentified, proteins contributes significantly to plant oxidative stress responses [3].

Associations of LSD1 with chemical compounds

• Salicylic acid, which induces stomatal closure, inhibits catalase activity and triggers the rcd phenotype in lsd1, also impaired acclimation of wild-type plants to conditions that promote EEE [5].
• This lsd1 mutant also had reduced stomatal conductance and catalase activity in short-day permissive conditions and induced H(2)O(2) accumulation followed by rcd when stomatal gas exchange was further impeded [5].
• Taken together, conditional PR-1 accumulation in lsd1 is regulated not by the redox state but by the endogenous level of glutathione [7].

Regulatory relationships of LSD1

• LSD1 regulates salicylic acid induction of copper zinc superoxide dismutase in Arabidopsis thaliana [1].

Other interactions of LSD1

• However, AtMYB30 expression could not be detected in the lsd1 mutant, which was hyper-responsive to cell death initiators and unable to limit the extent of cell death, whatever the environmental conditions [8].
• Here we demonstrate that a highly conserved LSD1 paralogue, LOL1, acts as a positive regulator of cell death [9].
• We also show that LSD1 and LOL1 have antagonistic effects on copper-zinc superoxide dismutase accumulation, consistent with functions in cell death control via maintenance of ROI homeostasis [9].
• Molecular analysis of programmed cell death during senescence in Arabidopsis thaliana and Brassica oleracea: cloning broccoli LSD1, Bax inhibitor and serine palmitoyltransferase homologues [10].

References