Central role of the LEAFY COTYLEDON1 transcription factor in seed development

Abstract

Seed development is a complex period of the flowering plant life cycle. After fertilization, the three main regions of the seed, embryo, endosperm and seed coat, undergo a series of developmental processes that result in the production of a mature seed that is developmentally arrested, desiccated, and metabolically quiescent. These processes are highly coordinated, both temporally and spatially, to ensure the proper growth and development of the seed. The transcription factor, LEAFY COTYLEDON1 (LEC1), is a central regulator that controls several aspects of embryo and endosperm development, including embryo morphogenesis, photosynthesis, and storage reserve accumulation. Thus, LEC1 regulates distinct sets of genes at different stages of seed development. Despite its critical importance for seed development, an understanding of the mechanisms underlying LEC1's multifunctionality is only beginning to be obtained. Recent studies describe the roles of specific transcription factors and the hormones, gibberellic acid and abscisic acid, in controlling the activity and transcriptional specificity of LEC1 across seed development. Moreover, studies indicate that LEC1 acts as a pioneer transcription factor to promote epigenetic reprogramming during embryogenesis. In this review, we discuss the mechanisms that enable LEC1 to serve as a central regulator of seed development.

Experiencing winter for spring flowering: A molecular epigenetic perspective on vernalization

“…The molecular epigenetic mechanisms underlying FLC regulation in Arabidopsis at different growth and development stages or in different seasons under natural conditions in temperate climates provide insights on how vernalization‐responsive crucifers synchronize their growth and development with seasonal changes (Figure 1). The FRI‐FLC regulatory module, the LEC pathway and VAL1 are evolutionarily conserved across the crucifer family (Suzuki and McCarty, 2008; Amasino 2010; Lepiniec et al 2018; Xie et al 2018; Jo et al 2019). Hence, overwintering crucifer annuals or biennials conceivably employ the FRI supercomplex, the embryonic LEC pathway, VAL1/2 and diverse chromatin modifiers (both active and repressive ones) to dynamically control (switch on/off) the expression of FLC homologs at different developmental stages through their life cycles to align with seasonal changes, particularly in temperate climates.…”

The role of light in regulating seed dormancy and germination

“…Seed maturation is characterized by the accumulation of storage reserves in the embryos. Dormancy (quiescent state) is induced during this phase (Yan and Chen 2017;Jo et al 2019). Subsequently, fully matured seeds enter an afterripening phase (desiccation stage), in which the dormancy level is gradually decreased and dry seeds become competent for germination (Angelovici et al 2010).…”

“…Other factors involved in light-induced regulation of seed dormancy induction and maintenance Various other transcription factors regulate the induction and maintenance of seed dormancy. LEAFY COTYLEDON1 (LEC1), LEC2, FUSCA3 (FUS3), and ABI3 are the four master regulators of seed maturation and dormancy induction (Yan and Chen 2017;Jo et al 2019). These regulators interact as a network to induce seed dormancy (To et al 2006).…”

The B3-Domain Transcription Factor VAL1 Regulates the Floral Transition by Repressing FLOWERING LOCUS T

“…Structural analysis of VAL1-B3 indicated that it forms H-bonds with all six bp in the RY motif (Sasnauskas et al, 2018). In addition to the B3 DNA-binding domain, VALs contain three other domains, including the PHD-like (PHD-L) and cysteine and tryptophan residue-containing (CW) domains (which are associated with histone binding) and the ethylene-responsive element binding factor-associated amphiphilic repression (EAR) domain (Suzuki and McCarty, 2008;Jo et al, 2019). PHD-L reads the methylation state of histone H3K27, whereas the CW domain is responsible for the interaction between VAL1 and HISTONE DEACETYLASE19 (Zhou et al, 2013;Yuan et al, 2016).…”