背景回顾：In Arabidopsis thaliana, the female gametophyte consists of two synergid cells, an egg cell, a diploid central cell, and three antipodal cells. CYTOKININ INDEPENDENT 1 (CKI1), a histidine kinase constitutively activating the cytokinin signaling pathway, specifies the central cell and restricts the egg cell. 

提出问题：However, the mechanism regulating CKI1-dependent central cell specification is largely unknown. 

结果1-蛋白定位：Here, we showed that the type-B ARABIDOPSIS RESPONSE REGULATORS10, 12, and 18 (ARR10/12/18) localize at the chalazal pole of the female gametophyte. 

结果2-功能分析：Phenotypic analysis showed that the arr10 12 18 triple mutant is female sterile. We examined the expression patterns of embryo sac marker genes and found that the embryo sac of arr10 12 18 plants had lost central cell identity, a phenotype similar to that of the Arabidopsis cki1 mutant. 

结果3-作用机制：Genetic analyses demonstrated that ARR10/12/18, CKI1, and ARABIDOPSIS HISTIDINE PHOSPHOTRANSFER PROTEIN2, 3, and 5 (AHP2/3/5) function in a common pathway to regulate female gametophyte development. In addition, constitutively activated ARR10/12/18 in the cki1 embryo sac partially restored the fertility of cki1. 

结果4-组学数据：Results of transcriptomic analysis supported the conclusion that ARR10/12/18 and CKI1 function together to regulate the identity of the central cell. 

结论：Our results demonstrated that ARR10/12/18 function downstream of CKI1–AHP2/3/5 as core factors to determine cell fate of the female gametophyte.

Activated ARR10/12/18 partially rescue the fertility of cki1.

在拟南芥中，雌配子体由2个助细胞、1个卵细胞、1个二倍体的中央细胞以及3个反足细胞组成。组氨酸激酶CKI1能够组成型激活细胞分裂素信号转导途径，特化中央细胞并限制卵细胞。但是，调控CKI1依赖型中央细胞特化的分子机制在很大程度上还是未知的。本文中，作者发现type-B ARR10/12/18定位于雌配子体的合点极。表型分析显示，arr10 12 18三突植株是雌性不育的。作者鉴定了胚囊标记基因的表达模式，发现arr10 12 18三突植株中胚囊丢失了中央细胞特征，该表型与cki1突变体的表型类似。遗传分析显示，ARR10/12/18、CKI1和AHP2/3/5在同一个通路上发挥功能，共同作用于雌配子体发育的调控。另外，cki1突变体胚囊中组成型激活ARR10/12/18能够恢复cki1突变体的育性。转录组分析的结果也支持ARR10/12/18和CKI1共同作用于中央细胞的命运特化。本文的研究结果揭示了ARR10/12/18作用于CKI1–AHP2/3/5的下游，是决定雌配子体细胞命运的核心因子。

** 苟小平 **