The maternal control of progeny seed physiology

在植物生态学中，人们早就认识到母株具有“赌注对冲”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，以最大限度地提高传播和成功繁殖后代的机会。这样的策略可能会以牺牲一些个体后代种子的生命机会为代价，因此已经假设在母亲的最佳传播和萌发策略与任何单个后代种子的最佳传播和萌发策略之间存在冲突。这一冲突在种子休眠控制过程中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性问题。众所周知，种子的严格的母体组织，如种皮，在休眠和传播中起着重要的作用。最近，已经清楚的是胚乳在休眠控制中起着关键作用，并且胚乳具有有利于母体的2：1的基因剂量偏差。此外，雌性和雄性生殖系中的特定表观遗传过程可以沉默来自一个亲本的等位基因，并且已知这些过程在种子发育中起重要作用。最近的一项研究暗示这些过程中的一些休眠控制，但很少有人知道母亲是否可以施加实质性的控制后代发芽行为，通过影响胚乳physiology.Polycomb抑制复合物2（PRC 2）的功能是一个重要因素，在母亲控制种子发育，通过沉积的表观遗传标记H3 K27 me 3。PRC 2基因在种子中的缺失导致母体效应种子败育，这部分是由于MADS盒家族转录因子在胚乳发育早期的失调所致。PRC 2需要特定的因子来将复合物靶向特定的基因座，并且已知在开花时间期间通过温度PHD家族转录因子控制对于该任务是重要的。值得注意的是，我们已经发现，这个小PHD-指子家族，VEL 2和VEL 3，这是相邻的拟南芥基因组中，有牵连的GWAS在控制种子休眠的温度。此外，我们发现，Vel 3突变体表现出母系遗传的种子萌发表型和PRC 2复杂mutants.This proposal描述了一个工作计划，旨在了解VEL家族PHD手指因子使种子休眠控制的母体植物的分子机制。通过一系列相互关联的目标，我们的目标是在分子水平上理解为什么VEL 3起母性作用，以及它的功能是否与VEL 2共享。我们将研究VEL 2/3是否与PRC 2复合体相关，鉴定其靶基因并测试这些基因是否受H3 K27 me 3沉积的调控。通过比较野生型和vel 3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状子叶1（LEC 1）的主调节转录因子控制休眠的假设。通过这种方式，我们的目标是描述一种分子途径，通过这种途径，母株保留后代种子生理学的控制，并测试在这一过程中是否发生自然变异拟南芥种质。

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.