A Mini-Review on Candidate Genes for Regulation of Reproduction and Puberty Onset

Iffat Fatima

doi:10.31031/prm.2018.03.000552

Abstract

Initiation and progression of puberty is a critical event for mammals. Various neuronal and hormonal cues are required for normal onset of puberty. GnRH is the major hormone involved in regulation of these mechanisms. Regulation of this complex process is controlled by multiple genes which encode respective proteins used as stimulatory inputs like glutamate, kisspeptin etc. or inhibitory inputs. These genes include KISS1/Kiss1, KISSR, Kissr, Tac3, TacR3, LEP, EAP1 etc.

Highlights

The pulsatile release of Gonadotropin releasing hormone (GnRH) from hypothalamus is essential for induction of initiation and progression of puberty in mammals
A network of neurons located in the medial basal hypothalamus (MBH) in primates is the source of GnRH release into portal vessels which makes a connection between brain and pituitary gland
Evidences from various puberty related defects support the significance of the respective genes in puberty onset. These include GnRH1, GnRHR, KISS1, KISS1R, Tac3, TacR3, Eap1, Lin28, LH receptor gene and FSH receptor gene etc. It can be exemplified by loss of function mutations in KISSR in humans result in isolated hypogonadotropic hypogonadism (IHH) whereas, gain of function mutations can lead to CPP [3]

Summary

Introduction

The pulsatile release of GnRH from hypothalamus is essential for induction of initiation and progression of puberty in mammals. Alterations in neuronal and glial inputs to GnRH producing neurons control its periodic secretion. Regulatory mechanisms of this process at transcriptional level are not well understood, but it is apparent that several genes are involved [1]. Evidences from various puberty related defects support the significance of the respective genes in puberty onset These include GnRH1, GnRHR, KISS1, KISS1R, Tac, TacR3, Eap, Lin, LH receptor gene and FSH receptor gene etc. It can be exemplified by loss of function mutations in KISSR in humans result in IHH whereas, gain of function mutations can lead to CPP (central precocious puberty) [3]

Findings

Discussion

Conclusion