Embryogenesis of flowering plants is initiated by polarization of the zygote, a prerequisite for correct axis formation in the embryo. The daughter cells of the asymmetric zygote division form the pro-embryo and the mostly extra-embryonic suspensor.¹ The suspensor plays a pivotal role in nutrient and hormone transport and rapid growth of the embryo.^2,3 Zygote polarization is controlled by a MITOGEN-ACTIVATING PROTEIN (MAP) kinase signaling pathway including the MAPKK kinase (MAP3K) YODA (YDA)⁴ and the upstream membrane-associated proteins BRASINOSTEROID SIGNALING KINASE 1 (BSK1) and BSK2.^5,6 Furthermore, suspensor development is controlled by cysteine-rich peptides of the EMBRYO SURROUNDING FACTOR 1 (ESF1) family.⁷ While they act genetically upstream of YDA, the corresponding receptor to perceive these potential ligands is unknown. In other developmental processes, such as stomata development, YDA activity is controlled by receptor kinases of the ERECTA family (ERf).8, 9, 10, 11, 12 While the receptor kinases upstream of BSK1/2 in the embryo have so far not been identified,¹ YDA is in part activated by the sperm cell-derived BSK family member SHORT SUSPENSOR (SSP) that represents a naturally occurring, constitutively active variant of BSK1.^5,13 It has been speculated that SSP might be a paternal component of a parental tug-of-war controlling resource allocation toward the embryo.^2,13 Here, we show that in addition to SSP, the receptor kinase ERECTA plays a crucial role in zygote polarization as a maternally contributed part of the embryonic YDA pathway. We conclude that two independent parental contributions initiate zygote polarization and control embryo development.

开花植物的胚胎发生是由受精卵的极化引发的，这是胚胎中正确形成轴的先决条件。不对称合子分裂的子细胞形成原胚和大部分胚外胚柄。¹胚柄在营养和激素运输以及胚胎的快速生长中起关键作用。^{2 , 3}受精卵极化受促分裂原激活蛋白 (MAP) 激酶信号通路控制，包括 MAPKK 激酶 (MAP3K) YODA (YDA) ⁴和上游膜相关蛋白 BRASINOSTEROID 信号激酶 1 (BSK1) 和 BSK2。^{5 , 6}此外，胚柄发育受胚胎周围因子 1 (ESF1) 家族的富含半胱氨酸的肽控制。⁷虽然它们在 YDA 的基因上游起作用，但感知这些潜在配体的相应受体是未知的。在其他发育过程中，例如气孔发育，YDA 活性由 ERECTA 家族 (ERf) 的受体激酶控制。8、9、10、11、12 而胚胎中 BSK1/2 上游的受体激酶迄今尚未已确定，¹ YDA 部分由精细胞衍生的 BSK 家族成员 SHORT SUSPENSOR (SSP) 激活，该成员代表 BSK1 的天然存在的组成型活性变体。^{5 , 13}据推测，SSP 可能是父母拔河比赛控制胚胎资源分配的父亲组成部分。^{2 , 13}在这里，我们表明，除了 SSP 之外，受体激酶 ERECTA 作为胚胎 YDA 途径的母体贡献部分在受精卵极化中起着至关重要的作用。我们得出结论，两个独立的父母贡献启动了受精卵极化并控制胚胎发育。