The Drosophila nuclear lamina protein otefin is required for germline stem cell survival.
The Drosophila nuclear lamina protein otefin is required for germline stem cell survival.
复制标题
DOI：
10.1016/j.devcel.2013.05.023
复制
发表时间：
2013-06-24
影响因子：
11.8
通讯作者：
Geyer, Pamela K.
中科院分区：
文献类型：
--
作者：
Barton, Lacy J.;Pinto, Belinda S.;Wallrath, Lori L.;Geyer, Pamela K.
LEM结构域（LEM-D）蛋白是广泛的蛋白质网络的组成部分，该网络在内核被膜下组装。LEM-D蛋白缺陷导致与干细胞稳态改变相关的组织限制性人类疾病。Otefin（Ote）是果蝇LEM-D蛋白，其本质上是维持雌性生殖系干细胞（GSC）所必需的。先前的研究将Ote损失与关键分化基因大理石袋（bag-of-marbles，bam）的转录激活联系起来，导致Ote将bam基因拴在核外围以进行基因沉默的模型。使用多个ote −/−背景的遗传和表型分析，我们获得了与该模型不一致的证据。我们发现，bam抑制在ote −/− GSC中维持，而生殖细胞损失在ote −/−，bam −/−突变体中持续存在，这表明GSC损失独立于bam转录。我们发现ote −/− GSCs的主要缺陷是分化受阻，最终导致生殖细胞死亡。
LEM domain (LEM-D) proteins are components of an extensive protein network that assembles beneath the inner nuclear envelope. Defects in LEM-D proteins cause tissue-restricted human diseases associated with altered stem cell homeostasis. Otefin (Ote) is a Drosophila LEM-D protein that is intrinsically required for female germline stem cells (GSCs) maintenance. Previous studies linked Ote loss with transcriptional activation of the key differentiation gene, bag-of-marbles (bam), leading to the model that Ote tethers the bam gene to the nuclear periphery for gene silencing. Using genetic and phenotypic analyses of multiple ote−/− backgrounds, we obtained evidence that is inconsistent with this model. We show that bam repression is maintained in ote−/− GSCs and that germ cell loss persists in ote−/−, bam−/− mutants, together demonstrating that GSC loss is independent of bam transcription. We show the primary defect in ote−/− GSCs is a block of differentiation, which ultimately leads to germ cell death.
登录
查看更多内容
影响因子：
10.5
作者：
MCKEARIN, DM;SPRADLING, AC
通讯作者：
SPRADLING, AC
影响因子：
11.4
作者：
Cai, ML;Huang, Y;Clore, GM
通讯作者：
Clore, GM
影响因子：
4.8
作者：
Mansharamani, M;Wilson, KL
通讯作者：
Wilson, KL
影响因子：
11.4
作者：
Markiewicz, Ewa;Tilgner, Katarzyna;Hutchison, Christopher J.
通讯作者：
Hutchison, Christopher J.
影响因子：
64.8
作者：
LASKO, PF;ASHBURNER, M
通讯作者：
ASHBURNER, M