Hamada-Kawaguchi Noriko, Yamamoto Daisuke
Division of Neurogenetics, Tohoku University Graduate School of Life Sciences, Katahira, Aoba-ku, Sendai, 980-8577, Japan.
Genesis. 2017 Aug;55(8). doi: 10.1002/dvg.23042. Epub 2017 Jul 19.
Drosophila Btk29A is a Tec family nonreceptor tyrosine kinase, the ortholog of which causes X-linked agammaglobulinemia in humans when mutant. In Btk29A mutant ovaries, multiple defects are observed: extrapolar cells form ectopically; osk mRNA fails to accumulate posteriorly in mature oocytes; the shape and alignment of follicle cells are grossly distorted. All these phenotypes are rescued by selectively overexpressing the type 2 isoform of wild-type Btk29A in follicle cells. Expression of certain proteins enriched in adherens junctions is markedly affected in Btk29A mutants; the anterior-posterior gradient normally observed in the expression of DE-Cadherin and Armadillo are lost and Canoe is sequestered from adherens junctions. Intriguingly, tyrosine phosphorylation of Canoe is reduced in Btk29A mutants. It is proposed that Btk29A is required for the establishment of egg chamber polarity presumably through the regulation of subcellular localization of its downstream proteins, including Cno.
果蝇Btk29A是一种Tec家族非受体酪氨酸激酶，其直系同源基因在人类中发生突变时会导致X连锁无丙种球蛋白血症。在Btk29A突变体卵巢中，观察到多种缺陷：极外细胞异位形成；osk mRNA在成熟卵母细胞中无法在后部积累；卵泡细胞的形状和排列严重扭曲。通过在卵泡细胞中选择性过表达野生型Btk29A的2型异构体，所有这些表型都得到了挽救。在Btk29A突变体中，某些富集于黏着连接的蛋白质的表达受到显著影响；通常在DE-钙黏蛋白和犰狳蛋白表达中观察到的前后梯度消失，并且Canoe从黏着连接中被隔离。有趣的是，在Btk29A突变体中，Canoe的酪氨酸磷酸化减少。有人提出，Btk29A可能通过调节其下游蛋白质（包括Cno）的亚细胞定位来建立卵室极性。
