Mechanisms underlying vernalization-mediated VIN3 induction in Arabidopsis

Abstract

VERNALIZATION INSENSITIVE 3 (VIN3) is required for vernalization-mediated repression of FLOWERING LOCUS C (FLC) in Arabidopsis. The induction of VIN3 by long-term exposure to cold is one of earliest events in vernalization response. However, molecular mechanisms underlying for the VIN3 induction are poorly understood. Recently, we reported that the constitutive repression of VIN3 in the absence of the cold exposure is due to multiple repressive chromatin modifying components, including a transposable element (TE)-derived sequence, LIKE-HETEROCHROMATIN PROTEIN 1 (LHP1) and POLYCOMB REPRESSION COMPLEX 2 (PRC2). In addition, the maximum level of VIN3 induction requires EARLY FLOWERING 7 (ELF7) and EARLY FLOWERING IN SHORDAYS (EFS), which are components of activating chromatin modifying complexes. Furthermore, dynamic changes in histone modifications at VIN3 chromatin are observed during the course of vernalization. Thus, mechanisms underlying the induction of VIN3 include changes at the level of chromatin.

Figure 1

Common regulatory networks to control the VIN3-FLC-FT pathway to control flowering time by vernalization. Common repression and activation complexes are likely involved in regulations of VIN3, FLC and FT. Bivalent chromatin status at VIN3 chromatin is achieved by vernalizing cold, resulting in transient induction of VIN3.