A Mutation in the Catalytic Subunit of the Glycosylphosphatidylinositol Transamidase Disrupts Growth, Fertility, and Stomata Formation
A Mutation in the Catalytic Subunit of the Glycosylphosphatidylinositol Transamidase Disrupts Growth, Fertility, and Stomata Formation
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DOI：
10.1104/pp.16.00339
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发表时间：
2016-06-01
期刊：
影响因子：
7.4
通讯作者：
Shpak, Elena D.
中科院分区：
文献类型：
--
作者：
Bundy, Mark G. R.;Kosentka, Pawel Z.;Shpak, Elena D.
GPI锚定蛋白（GPI-AP）是植物生长发育所必需的蛋白质，对负责锚生物合成或附着的酶基因敲除突变会对配子体或胚致死。在一个基因筛选的目标，以确定调控气孔形成的基因，我们发现了一个错义突变的拟南芥（拟南芥）同源GPI 8/PIG-K，半胱氨酸蛋白酶，转移组装GPI锚蛋白。拟南芥基因组中只有一个AtGPI 8拷贝，atgpi 8 -1突变降低了这种酶的效率，导致GPI锚定蛋白的积累减少。虽然atgpi 8 -1突变强烈破坏植物生长，但它不是致命的。atgpi 8 -1突变体的表型分析表明，GPI-AP是重要的根和芽的生长，气孔形成，顶端优势，过渡到开花，和雄配子体的活力。此外，atgpi 8 -1突变体积累更高水平的胼胝质，并具有降低的胞间连丝渗透性。atgpi 8 -1与ERECTA家族（ERf）基因突变的遗传相互作用表明在调节气孔形成的ERf信号传导途径的分支中存在GPI-AP。组成型活性YODA激活ERf信号转导级联拯救atgpi 8 -1中的气孔簇，表明GPI-AP在MAP激酶级联的上游起作用。TMM是一种能与ERfs形成异源二聚体的受体样蛋白。我们的分析表明，tmm-1是上位的atgpi 8 -1，表明要么TMM是一个GPI-AP或有另一个GPI-AP调节气孔发育，其功能是依赖于TMM。
GPI-anchored proteins (GPI-APs) are essential for plant growth and development; knockout mutations in enzymes responsible for anchor biosynthesis or attachment are gametophyte or embryo lethal. In a genetic screen targeted to identify genes regulating stomata formation, we discovered a missense mutation in the Arabidopsis (Arabidopsis thaliana) homolog of GPI8/PIG-K, a Cys protease that transfers an assembled GPI anchor to proteins. The Arabidopsis genome has a single copy of AtGPI8, and the atgpi8-1 mutation reduces the efficiency of this enzyme, leading to reduced accumulation of GPI-anchored proteins. While the atgpi8-1 mutation strongly disrupts plant growth, it is not lethal. Phenotypic analysis of atgpi8-1 mutants suggests that GPI-APs are important for root and shoot growth, stomata formation, apical dominance, transition to flowering, and male gametophyte viability. In addition, atgpi8-1 mutants accumulate higher levels of callose and have reduced plasmodesmata permeability. Genetic interactions of atgpi8-1 with mutations in ERECTA family (ERf) genes suggest the existence of a GPI-AP in a branch of the ERf signaling pathway that regulates stomata formation. Activation of the ERf signal transduction cascade by constitutively active YODA rescues stomata clustering in atgpi8-1, indicating that a GPI-AP functions upstream of the MAP kinase cascade. TOO MANY MOUTHS (TMM) is a receptor-like protein that is able to form heterodimers with ERfs. Our analysis demonstrates that tmm-1 is epistatic to atgpi8-1, indicating that either TMM is a GPI-AP or there is another GPI-AP regulating stomata development whose function is dependent upon TMM.