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Differential regulation of Kit ligand A expression in the ovary by IGF-I via different pathways.

ABSTRACT: Kit ligand (KITL) plays indispensable roles both in primordial follicle activation and in the maintenance of meiotic arrest of the oocyte. The regulation of KITL expression in the ovary, however, remains largely unknown. In the zebrafish, there are 2 paralogues of KITL, kitlga and kitlgb, and 2 Kit receptors, kita and kitb. Consistent with the situation in mammals, kitlga is only expressed in the ovarian follicle cells, and its cognate receptor kita is expressed in the oocyte. In the present study, we demonstrated that the expression of kitlga was promoted by IGF-I through its receptor IGF-IR. The stimulation involved transcription but not translation, suggesting that the kitlga gene is likely a direct downstream target of IGF-I signaling. Further experiments showed that the stimulatory effect of IGF-I was mediated by phosphatidyl inositol 3-kinase (PI3K)-Akt pathway. IGF-I also activated MEK-ERK pathway; however, this pathway suppressed kitlga expression. The regulation of kitlga expression by IGF-I appeared to depend on the stage of follicle development with a greater induction at early stage than late stage. This may be related to changes in IGF-I signaling pathways and/or local paracrine environment. In support of this were the differential expression of IGF-I receptors (igf1ra and igf1rb) and responsiveness of IGF-I signaling pathways, especially the PI3K-Akt pathway. Furthermore, the IGF-I-induced kitlga expression was inhibited by epidermal growth factor, an oocyte-derived paracrine factor in the zebrafish follicle. This study provides evidence for a controlling mechanism underlying the regulation of KITL expression in the ovary.

SUBMITTER: Yao K

PROVIDER: S-EPMC5426649 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature

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Differential regulation of Kit ligand A expression in the ovary by IGF-I via different pathways.

Yao Kai K Lau Shuk-Wa SW Ge Wei W

Molecular endocrinology (Baltimore, Md.) 20131121 1

Kit ligand (KITL) plays indispensable roles both in primordial follicle activation and in the maintenance of meiotic arrest of the oocyte. The regulation of KITL expression in the ovary, however, remains largely unknown. In the zebrafish, there are 2 paralogues of KITL, kitlga and kitlgb, and 2 Kit receptors, kita and kitb. Consistent with the situation in mammals, kitlga is only expressed in the ovarian follicle cells, and its cognate receptor kita is expressed in the oocyte. In the present stu ...[more]

PMID: 24243489

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Project description:The retention of particular genes after the whole genome duplication in zebrafish has given insights into how genes may evolve through partitioning of ancestral functions. We examine the partitioning of expression patterns and functions of two zebrafish kit ligands, kit ligand a (kitla) and kit ligand b (kitlb), and discuss their possible coevolution with the duplicated zebrafish kit receptors (kita and kitb). In situ hybridizations show that kitla mRNA is expressed in the trunk adjacent to the notochord in the middle of each somite during stages of melanocyte migration and later expressed in the skin, when the receptor is required for melanocyte survival. kitla is also expressed in other regions complementary to kita receptor expression, including the pineal gland, tail bud, and ear. In contrast, kitlb mRNA is expressed in brain ventricles, ear, and cardinal vein plexus, in regions generally not complementary to either zebrafish kit receptor ortholog. However, like kitla, kitlb is expressed in the skin during stages consistent with melanocyte survival. Thus, it appears that kita and kitla have maintained congruent expression patterns, while kitb and kitlb have evolved divergent expression patterns. We demonstrate the interaction of kita and kitla by morpholino knockdown analysis. kitla morphants, but not kitlb morphants, phenocopy the null allele of kita, with defects for both melanocyte migration and survival. Furthermore, kitla morpholino, but not kitlb morpholino, interacts genetically with a sensitized allele of kita, confirming that kitla is the functional ligand to kita. Last, we examine kitla overexpression in embryos, which results in hyperpigmentation caused by an increase in the number and size of melanocytes. This hyperpigmentation is dependent on kita function. We conclude that following genome duplication, kita and kitla have maintained their receptor-ligand relationship, coevolved complementary expression patterns, and that functional analysis reveals that most or all of the kita receptor's function in the embryo are promoted by its interaction with kitla.

Dataset Information

Differential regulation of Kit ligand A expression in the ovary by IGF-I via different pathways.

Publications

Differential regulation of Kit ligand A expression in the ovary by IGF-I via different pathways.

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