Redundancy in Kiss1 expression safeguards reproduction in the mouse.
نویسندگان
چکیده
Kisspeptin (Kiss1) signaling to GnRH neurons is widely acknowledged to be a prerequisite for puberty and reproduction. Animals lacking functional genes for either kisspeptin or its receptor exhibit low gonadotropin secretion and infertility. Paradoxically, a recent study reported that genetic ablation of nearly all Kiss1-expressing neurons (Kiss1 neurons) does not impair reproduction, arguing that neither Kiss1 neurons nor their products are essential for sexual maturation. We posited that only minute quantities of kisspeptin are sufficient to support reproduction. If this were the case, animals having dramatically reduced Kiss1 expression might retain fertility, testifying to the redundancy of Kiss1 neurons and their products. To test this hypothesis and to determine whether males and females differ in the required amount of kisspeptin needed for reproduction, we used a mouse (Kiss1-CreGFP) that has a severe reduction in Kiss1 expression. Mice that are heterozygous and homozygous for this allele (Kiss1(Cre/+) and Kiss1(Cre/Cre)) have ∼50% and 95% reductions in Kiss1 transcript, respectively. We found that although male Kiss1(Cre/Cre) mice sire normal-sized litters, female Kiss1(Cre/Cre) mice exhibit significantly impaired fertility and ovulation. These observations suggest that males require only 5% of normal Kiss1 expression to be reproductively competent, whereas females require higher levels for reproductive success.
منابع مشابه
Identification of Spata-19 New Variant with Expression beyond Meiotic Phase of Mouse Testis Development
Background: The study of specific genes expressed in the testis is important to understanding testis development and function. Spermatogenesis is an attractive model for the study of gene expression during germ cell differentiation. Spermatogenesis associated-19 (Spata-19) is a recently-identified important spermatogenesis-related gene specifically expressed in testis. Its protein product is in...
متن کاملHypothalamic Expression of KiSS1 and RFamide-related Peptide-3 mRNAs during The Estrous Cycle of Rats
متن کامل
The effect of intracerebroventricular administration of neuropeptide Y on reproductive axis function in the male Wistar rats: Involvement of hypothalamic KiSS1/GPR54 system
Several studies have shown that neuropeptide Y (NPY) is considered to be one of the key regulators of the hypothalamic-pituitary-gonadal axis in the mammals. Also, kisspeptin is a powerful upstream regulator of gonadotropin-releasing hormone neurons in the hypothalamus. The present study aims to investigate the effects of the intracerebroventricular (ICV) injection of NPY and BIBP3226 (NPY rece...
متن کاملExamination of the immunohistochemical localization and gene expression by RT-PCR of the oxytocin receptor in diabetic and non-diabetic mouse testis
Objective(s): The aim of this study was to determine Oxytocin receptor (OTR) gene expression and localization in diabetic and non-diabetic mouse testes by RT-PCR and immunohistochemistry, respectively. Materials and Methods: In this study, 18 male BALB/c mice (8–12 weeks old) were used and divided into three groups: diabetic, sham, and control. Streptozotocin (STZ) was applied to the diabetic g...
متن کاملPancreatic Differentiation of Sox 17 Knock-in Mouse Embryonic Stem Cells in Vitro
The way to overcome current limitations in the generation of glucose-responsive insulin-producing cells is selective enrichment of the number of definitive endoderm (DE) progenitor cells. Sox17 is the marker of mesendoderm and definitive endoderm. The aim of the present research was to study the potential of Sox17 knock-in CGR8 mouse embryonic stem (ES) cells to differentiate into insulin produ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Endocrinology
دوره 154 8 شماره
صفحات -
تاریخ انتشار 2013