Fertilization introduces parental genetic information into the zygote to guide embryogenesis. Parental contributions to postfertilization development have been discussed for decades, and the data available show that both parents contribute to the zygotic transcriptome, suggesting a paternal role in early embryogenesis^1,2,3,4,5,6. However, because the specific paternal effects on postfertilization development and the molecular pathways underpinning these effects remain poorly understood, paternal contribution to early embryogenesis and plant development has not yet been adequately demonstrated⁷. Here our research shows that TREE1 and its homologue DAZ3 are expressed exclusively in Arabidopsis sperm. Despite presenting no evident defects in sperm development and fertilization, tree1 daz3 unexpectedly led to aberrant differentiation of the embryo root stem cell niche. This defect persisted in seedlings and disrupted root tip regeneration, comparable to congenital defects in animals. TREE1 and DAZ3 function by suppression of maternal RKD2 transcription, thus mitigating the detrimental maternal effects from RKD2 on root stem cell niche. Therefore, our findings illuminate how genetic deficiencies in sperm can exert enduring paternal effects on specific plant organ differentiation and how parental-of-origin genes interact to ensure normal embryogenesis. This work also provides a new concept of how gamete quality or genetic deficiency can affect specific plant organ formation.

受精将亲本遗传信息引入受精卵以指导胚胎发生。几十年来，人们一直在讨论父母对受精后发育的贡献，现有数据显示父母双方都对合子转录组有贡献，这表明父系在早期胚胎发生中的作用^1,2,3,4,5,6。然而，由于父系对受精后发育的特定影响以及支撑这些影响的分子途径仍然知之甚少，因此父系对早期胚胎发生和植物发育的贡献尚未得到充分证明⁷。在这里，我们的研究表明 TREE1 及其同源物 DAZ3 仅在拟南芥精子中表达。尽管在精子发育和受精方面没有明显的缺陷，但 tree1 daz3 出乎意料地导致了胚胎根干细胞生态位的异常分化。这种缺陷在幼苗中持续存在并破坏了根尖再生，与动物的先天性缺陷相当。TREE1 和 DAZ3 通过抑制母体 RKD2 转录发挥作用，从而减轻 RKD2 对根干细胞生态位的有害母体影响。因此，我们的研究结果阐明了精子中的遗传缺陷如何对特定的植物器官分化产生持久的父系影响，以及亲本基因如何相互作用以确保正常的胚胎发生。这项工作还提供了一个关于配子质量或遗传缺陷如何影响特定植物器官形成的新概念。