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The Sm Core Protein SmEb Regulates Salt Stress Responses Through Maintaining Proper Splicing of RCD1 Pre-mRNA in Arabidopsis

ABSTRACT: Salt stress caused by soil salination inhibits plant growth and development that result in reduction of crop yield and threaten the food security. Several spliceosome components are considered to modify salt stress responses in plants. However, the molecular basis of spliceosome proteins adjustment to salt stress is still unclear. Here we report that an Sm core protein SmEb is required for salt tolerance in Arabidopsis. In addition, SmEb controls alternative splicing of hundreds of pre-mRNA to participate in plant response to salt stress. Our results further reveal that SmEb takes effect on maintain proper ratio of two RCD1 splicing variants to adjust to H2O2 accumulation under salt stress. Together, our findings uncover that proper alternative splicing of pre-mRNAs governed by the spliceosome component SmEb is essential for plant salt stress responses. Salt stress caused by soil salination inhibits plant growth and development that result in reduction of crop yield and threaten the food security. Several spliceosome components are considered to modify salt stress responses in plants. However, the molecular basis of spliceosome proteins adjustment to salt stress is still unclear. Here we report that an Sm core protein SmEb is required for salt tolerance in Arabidopsis. In addition, SmEb controls alternative splicing of hundreds of pre-mRNA to participate in plant response to salt stress. Our results further reveal that SmEb takes effect on maintain proper ratio of two RCD1 splicing variants to adjust to H2O2 accumulation under salt stress. Together, our findings uncover that proper alternative splicing of pre-mRNAs governed by the spliceosome component SmEb is essential for plant salt stress responses.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE208786 | GEO | 2023/04/01

REPOSITORIES: GEO

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Project description:Cold stress resulting from chilling and freezing temperatures substantially inhibits plant growth and reduces crop production worldwide. Tremendous research efforts have been focused on elucidating the molecular mechanisms of freezing tolerance in plants. Little is known about the molecular nature of chilling stress responses in plants. Here we found that two allelic mutants in a spliceosome component gene SmEb (smeb-1 and smeb-2) are defective in development and responses to chilling stress. RNA-seq analysis revealed that SmEb controls the splicing of many pre-mRNAs under chilling stress. The intron retentive COP1b splicing variant was dramatically induced by chilling stress in the smeb mutants. This nuclear-depleted COP1b lacks the nuclear speckle-localization capacity, supporting the regulatory role of COP1-HY5 interaction in hypocotyl elongation during chilling stress. Genetic evidence indicates that chilling-sensitive phenotype of the smeb mutants are partially rescued by the hy5 mutation. The transcription factor BES1 shows a dramatic defect in pre-mRNA splicing in the smeb mutants. Ectopic expression of the two BES1 splicing variants enhances the chilling sensitivity of the smeb-1 mutant. Biochemical and genetic analysis showed that CBFs act as negative upstream regulators of SmEb by directly suppressing its transcription. Together, our results demonstrate that proper alternative splicing of pre-mRNAs controlled by the spliceosome component SmEb is critical for plant development and chilling stress responses. Cold stress resulting from chilling and freezing temperatures substantially inhibits plant growth and reduces crop production worldwide. Tremendous research efforts have been focused on elucidating the molecular mechanisms of freezing tolerance in plants. Little is known about the molecular nature of chilling stress responses in plants. Here we found that two allelic mutants in a spliceosome component gene SmEb (smeb-1 and smeb-2) are defective in development and responses to chilling stress. RNA-seq analysis revealed that SmEb controls the splicing of many pre-mRNAs under chilling stress. The intron retentive COP1b splicing variant was dramatically induced by chilling stress in the smeb mutants. This nuclear-depleted COP1b lacks the nuclear speckle-localization capacity, supporting the regulatory role of COP1-HY5 interaction in hypocotyl elongation during chilling stress. Genetic evidence indicates that chilling-sensitive phenotype of the smeb mutants are partially rescued by the hy5 mutation. The transcription factor BES1 shows a dramatic defect in pre-mRNA splicing in the smeb mutants. Ectopic expression of the two BES1 splicing variants enhances the chilling sensitivity of the smeb-1 mutant. Biochemical and genetic analysis showed that CBFs act as negative upstream regulators of SmEb by directly suppressing its transcription. Together, our results demonstrate that proper alternative splicing of pre-mRNAs controlled by the spliceosome component SmEb is critical for plant development and chilling stress responses.

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The Sm Core Protein SmEb Regulates Salt Stress Responses Through Maintaining Proper Splicing of RCD1 Pre-mRNA in Arabidopsis

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