Abstract
BackgroundSimilar to other eukaryotes, splicing is emerging as an important process affecting development and stress tolerance in plants. Ski-interacting protein (SKIP), a splicing factor, is essential for circadian clock function and abiotic stress tolerance; however, the mechanisms whereby it regulates flowering time are unknown.ResultsIn this study, we found that SKIP is required for the splicing of serratedleaves and early flowering (SEF) pre-messenger RNA (mRNA), which encodes a component of the ATP-dependent SWR1 chromatin remodeling complex (SWR1-C). Defects in the splicing of SEF pre-mRNA reduced H2A.Z enrichment at FLC, MAF4, and MAF5, suppressed the expression of these genes, and produced an early flowering phenotype in skip-1 plants.ConclusionsOur findings indicate that SKIP regulates SWR1-C function via alternative splicing to control the floral transition in Arabidopsis thaliana.
Highlights
Similar to other eukaryotes, splicing is emerging as an important process affecting development and stress tolerance in plants
We focused on dissecting the mechanisms whereby Ski-interacting protein (SKIP) controls flowering time in Arabidopsis
SKIP activates the expression of FLOWERING LOCUS C (FLC) and its homologs to repress flowering Because the skip-1 mutation is insensitive to photoperiod, we examined the expression of CONSTANS (CO), a key regulator of photoperiodic flowering, in the skip-1 mutant [56]
Summary
Similar to other eukaryotes, splicing is emerging as an important process affecting development and stress tolerance in plants. Results: In this study, we found that SKIP is required for the splicing of serrated leaves and early flowering (SEF) pre-messenger RNA (mRNA), which encodes a component of the ATP-dependent SWR1 chromatin remodeling complex (SWR1-C). Defects in the splicing of SEF pre-mRNA reduced H2A.Z enrichment at FLC, MAF4, and MAF5, suppressed the expression of these genes, and produced an early flowering phenotype in skip-1 plants. Vernalization, the acceleration of flowering by prolonged cold, epigenetically silences FLC through the activity of polycomb repressive complex 2, In contrast, the PAF1 complex [11, 12], histone 2B ubiquitination [13, 14], histone 3 K4 and K36 methyltransferase complexes [15,16,17,18], the ATP-dependent SWR1 chromatin remodeling complex (SWR1-C) [19,20,21], and FRI/ FRI-like genes (e.g., FRL1 and FRL2) [22, 23] are involved in the activation of FLC to suppress the floral transition through chromatin modification or remodeling in Arabidopsis [2, 24]. The SWR1-C is required for H2A.Z deposition at FLC, MAF4, Cui et al BMC Biology (2017) 15:80 and MAF5 chromatin, which promotes transcription at these loci [21]
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