The maternal control of progeny seed physiology

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In plant ecology it has long been recognised that mother plants have 'bet-hedging' strategies, a mechanism to spread the germination behaviour of progeny seed in space and time to maximise the chances of dispersal and successful progeny reproduction. Such strategies can come at a cost to the life chances of some individual progeny seeds, and thus it has been hypothesised that conflict exists between the optimal dispersal and germination strategy for the mother and that of any single progeny seed. How and whether this conflict manifests itself at the molecular level during seed dormancy control is an important open question in plant reproductive biology. It is well known that the strictly maternal tissues of the seed, such as the seed coat, can play an important role in dormancy and dispersal. More recently, it has become clear that the endosperm plays a critical role in dormancy control, and the endosperm has a 2:1 gene dosage bias in favour of the mother. In addition, specific epigenetic processes in the female and male germline can silence alleles from one parent, and it is known that these processes play an important role in seed development. One recent study implicates some of these processes in dormancy control, but little is known of whether the mother can exert substantial control of progeny germination behaviour by influencing endosperm physiology.Polycomb Repressive Complex 2 (PRC2) function is an important factor in the maternal control of seed development, via deposition of the epigenetic mark H3K27me3. Loss of PRC2 in seeds leads to maternal effect seed abortion resulting in part from the deregulation of MADS box family transcription factors in early endosperm development. PRC2 requires specific factors to target the complex to specific loci, and during flowering time control by temperature PHD-family transcription factors are known to be important for this task. Notably, we have found that two of this small PHD-finger sub-family, VEL2 and VEL3, which lie adjacent in the Arabidopsis genome, are implicated by GWAS in the control of seed dormancy by temperature. In addition, we show that vel3 mutants exhibit a maternally-inherited seed germination phenotype and share some seed development phenotypes with PRC2 complex mutants.This proposal describes a workplan which aims to understand the molecular mechanism by which VEL-family PHD finger factors enable seed dormancy control by the mother plant. Through a series of linked objectives, we aim to understand at the molecular level why VEL3 acts maternally, and whether its function is shared by VEL2. We will investigate whether VEL2/3 associate with the PRC2 complex, identify their target genes and test whether these are regulated by H3K27me3 deposition. By building on transcriptome data comparing wild type and vel3 mutant endosperms, we will test the hypothesis that VEL proteins control dormancy through the master regulatory transcription factor of the seed maturation and dormancy programme leafy cotyledon 1 (LEC1). In this way we aim to describe a molecular pathway by which the mother plant retains control of progeny seed physiology, and test whether natural variation in this process occurs within Arabidopsis accessions.