Lee Kangseok, Pisarska Margareta D, Ko Jeong-Jae, Kang Yeongseup, Yoon Seongmin, Ryou Sang-Mi, Cha Kwang-Yul, Bae Jeehyeon
Department of Life Science, College of Natural Science, Chung-Ang University, Seoul 156-756, Republic of Korea.
Biochem Biophys Res Commun. 2005 Oct 28;336(3):876-81. doi: 10.1016/j.bbrc.2005.08.184.
Blepharophimosis-ptosis-epicanthus inversus syndrome type I is an autosomal disorder caused by mutations in FOXL2 gene and associated with premature ovarian failure in women by a dominant inheritance. FOXL2 is a recently identified protein that belongs to forkhead family transcription factor, of which signaling pathways are still unknown. Here, we show that FOXL2 induces apoptosis in both Chinese hamster ovary cells and rat granulosa cells, and it interacts with DP103, a DEAD box-containing protein. Overexpression of DP103 itself did not affect cell viability while its coexpression with FOXL2 led to the potentiation of cell death. Our results present previously undiscovered functions of these proteins, an apoptotic activity of FOXL2 in the ovary and a modulating activity of DP103 by interacting with FOXL2.
I型睑裂狭小-上睑下垂-内眦赘皮综合征是一种常染色体疾病，由FOXL2基因突变引起，通过显性遗传与女性的卵巢早衰相关。FOXL2是一种最近鉴定出的蛋白质，属于叉头家族转录因子，其信号通路尚不清楚。在此，我们表明FOXL2在中国仓鼠卵巢细胞和大鼠颗粒细胞中均诱导细胞凋亡，并且它与含DEAD框的蛋白质DP103相互作用。DP103自身的过表达不影响细胞活力，而其与FOXL2共表达导致细胞死亡增强。我们的结果揭示了这些蛋白质以前未被发现的功能，即FOXL2在卵巢中的凋亡活性以及DP103通过与FOXL2相互作用的调节活性。
