The maternal control of progeny seed physiology

在植物生态学中，人们很早就认识到，母植物有“更好的对冲”策略，这是一种在空间和时间上传播后代种子萌发行为的机制，以最大限度地扩大扩散和成功繁殖后代的机会。这样的策略可能会以某些个体后代种子的生命机会为代价，因此有人假设，母亲的最佳传播和萌发策略与任何单个子代种子的最佳传播和萌发策略之间存在冲突。在种子休眠控制过程中，这种冲突如何以及是否在分子水平上表现出来，是植物生殖生物学中一个重要的开放问题。众所周知，种子中严格意义上的母性组织，如种皮，在休眠和散布过程中起着重要作用。最近，胚乳在休眠控制中起着关键作用，并且胚乳对母亲有2：1的基因剂量偏向。此外，雌性和雄性生殖系中特定的表观遗传过程可以沉默来自一个亲本的等位基因，众所周知，这些过程在种子发育中发挥着重要作用。最近的一项研究表明，其中一些过程与休眠控制有关，但很少有人知道母亲是否能通过影响胚乳生理来对后代萌发行为施加实质性控制。多梳抑制复合体2(PRC2)的功能是通过沉积表观遗传标记H3K27me3而在母体控制种子发育的一个重要因素。种子中PRC2的缺失导致母性效应，导致种子败育，部分原因是胚乳发育早期MADS盒家族转录因子的失控。PRC2需要特定的因子将复合体靶向特定的基因座，而在开花期间，受温度控制的PhD家族转录因子对这一任务是重要的。值得注意的是，我们发现这个小的PhD-Finger亚家族中的两个，VEL2和VEL3，位于拟南芥基因组中的相邻位置，与GWAS有关，参与了温度对种子休眠的控制。此外，我们还发现，vel3突变体表现出母系遗传的种子萌发表型，并与prC2复合突变体具有相同的种子发育表型。本研究计划旨在了解Vel家族PHD指因子使母株控制种子休眠的分子机制。通过一系列相互关联的目标，我们的目标是在分子水平上了解VEL3为什么起母性作用，以及它的功能是否与VEL2共享。我们将调查VEL2/3是否与PRC2复合体相关，确定它们的靶基因，并测试这些基因是否受H3K27me3沉积的调节。通过比较野生型和vel3突变体胚乳的转录组数据，我们将检验VEL蛋白通过种子成熟和休眠程序叶子叶1(LEC1)的主调控转录因子来控制休眠的假说。通过这种方式，我们的目标是描述一种分子途径，通过它母株保持对后代种子生理的控制，并测试这一过程中的自然变异是否发生在拟南芥材料中。

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.