背景回顾：Endosperm is an angiosperm innovation central to their reproduction whose development, and thus seed viability, is controlled by genomic imprinting, where expression from certain genes is parent-specific. Unsuccessful imprinting has been linked to failed inter-specific and inter-ploidy hybridization. 

提出问题：Despite their importance in plant speciation, the underlying mechanisms behind these endosperm-based barriers remain poorly understood. 

主要研究：Here, we describe one such barrier between diploid Mimulus guttatus and tetraploid M. luteus. 

结果1-亲本差异：The two parents differ in endosperm DNA methylation, expression dynamics, and imprinted genes. 

结果2-杂交种子败育表型：Hybrid seeds suffer from underdeveloped endosperm, reducing viability, or arrested endosperm and seed abortion when M. guttatus or M. luteus is seed parent, respectively, and transgressive methylation and expression patterns emerge. 

结果3-杂交种子败育机理：The two inherited M. luteus subgenomes, genetically distinct but epigenetically similar, are expressionally dominant over the M. guttatus genome in hybrid embryos and especially their endosperm, where paternal imprints are perturbed. In aborted seeds, de novo methylation is inhibited, potentially owing to incompatible paternal instructions of imbalanced dosage from M. guttatus imprints. 

结论：We suggest that diverged epigenetic/regulatory landscapes between parental genomes induce epigenetic repatterning and global shifts in expression, which, in endosperm, may uniquely facilitate incompatible interactions between divergent imprinting schemes, potentially driving rapid barriers.

 摘 要 

胚乳是被子植物的一种创新，对于被子植物的繁殖至关重要，其发育和种子活力受基因组印记控制，即其中某些基因的表达具有亲本特异性。不成功的印记与种间和倍体间杂交不亲和有关。尽管其在植物物种形成中具有重要意义，但这些胚乳相关屏障背后的潜在机制仍不清楚。本文中，作者发现二倍体斑点沟酸浆（Mimulus guttatus）和四倍体锦花沟酸浆（M. luteus）之间就存在这样的胚乳屏障。这两个亲本在胚乳DNA甲基化、表达动态和印记基因方面存在明显差异。当斑点沟酸浆和锦花沟酸浆分别作为亲本一方时，获得的杂交种子存在胚乳发育不良、生活力下降，或胚乳停滞、种子败育的现象，并且出现超亲甲基化和表达模式。从四倍体锦花沟酸浆遗传的两套亚基因组在遗传上是不同的，但是表观上相似，并且在杂交的胚中对来自二倍体斑点沟酸浆的基因组呈表达显性，并且胚乳中亲本印记受到的干扰。在停止发育的种子中，从头甲基化受到抑制，可能是由于来自二倍体斑点沟酸浆的剂量不平衡所导致的不相容亲本指令。作者提出，亲本基因组之间的表观/调控的景观分化诱导表观模式重建和表达整体变化，而这在胚乳中可能独特地促进了分化印记间的不相容互作，从而可能驱动快速的胚乳障碍。