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]

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Summary

Introduction

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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