Talk:Genital System Development

About Discussion Pages

On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes: References - recent and historic that relates to the topic Additional topic information - currently prepared in draft format Links - to related webpages Topic page - an edit history as used on other Wiki sites Lecture/Practical - student feedback Student Projects - online project discussions. Links: Pubmed Most Recent | Reference Tutorial | Journal Searches Glossary Links Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link Cite this page: Hill, M.A. (2024, April 19) Embryology Genital System Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Genital_System_Development

2012

Sex determination strategies in 2012: towards a common regulatory model?

Reprod Biol Endocrinol. 2012 Feb 22;10:13.

Angelopoulou R, Lavranos G, Manolakou P. Source Experimental Embryology Unit, Department of Histology and Embryology, Medical School, Athens University, Athens, Greece. rangelop@med.uoa.gr

Abstract

Sex determination is a complicated process involving large-scale modifications in gene expression affecting virtually every tissue in the body. Although the evolutionary origin of sex remains controversial, there is little doubt that it has developed as a process of optimizing metabolic control, as well as developmental and reproductive functions within a given setting of limited resources and environmental pressure. Evidence from various model organisms supports the view that sex determination may occur as a result of direct environmental induction or genetic regulation. The first process has been well documented in reptiles and fish, while the second is the classic case for avian species and mammals. Both of the latter have developed a variety of sex-specific/sex-related genes, which ultimately form a complete chromosome pair (sex chromosomes/gonosomes). Interestingly, combinations of environmental and genetic mechanisms have been described among different classes of animals, thus rendering the possibility of a unidirectional continuous evolutionary process from the one type of mechanism to the other unlikely. On the other hand, common elements appear throughout the animal kingdom, with regard to a) conserved key genes and b) a central role of sex steroid control as a prerequisite for ultimately normal sex differentiation. Studies in invertebrates also indicate a role of epigenetic chromatin modification, particularly with regard to alternative splicing options. This review summarizes current evidence from research in this hot field and signifies the need for further study of both normal hormonal regulators of sexual phenotype and patterns of environmental disruption. © 2012 Angelopoulou et al; licensee BioMed Central Ltd.

PMID 22357269

Table 1
Regulatory elements in sex determination/dosage compensation
Species	Worms	Insects	Reptiles	Amphibians	Fish	Birds	Mammals
Epigenetic phenomena	unknown	alternative splicing	unknown	unknown	unknown	unknown	X inactivation
Primary sex determination	cellular	all tissues	gonad	gonad	gonad	all tissues	gonad
Role of sex steroids	unclear	unclear	sex det.	sex diff.	sex diff.	sex diff.	sex diff.
Role of Temperature	unclear	TSD (rare)	TSD	TSD	TSD	none	none
Sex chromosomes	X, W	X(Y) ZZ/ZW	ZZ/ZWXX/XY	ZZ/ZW (Xenopus)	XX/XYZZ/ZW	ZZ/ZW	XX/XY
Sex determining gene(s)	her-1, fem, tra	SXL	no	DM-W	DMY	DMRT1	SRY
Major regulatory elements in sex determination systems across the animal kingdom. Extensive similarities are noted even among distant species. Sex det: sex determination, Sex diff: Sex differentiation TSD: temperature-sensitive sex determination
Angelopoulou et al. Reproductive Biology and Endocrinology 2012 10:13 doi:10.1186/1477-7827-10-13

2009

Development of the human Müllerian duct in the sexually undifferentiated stage

An embryological explanation for the development of the Müllerian duct still poses a major challenge. The development of this duct was investigated systematically in human embryos. Seven embryos (Carnegie stages 18-23) were serially sectioned in the frontal, sagittal, and transversal planes at a thickness of 10 microm and stained with hematoxylin and eosin (H&E) for histological analysis. In all observed embryos, the caudal end of the Müllerian duct was found to be intimately connected to the Wolffian duct. The opening of the Müllerian duct to the coelomic cavity was formed as the result of an invagination of the coelomic epithelium at Carnegie stage 18. The duct grew independently from the invagination during stages 19-23. The fused duct (uterovaginal canal) bifurcated at the caudal portion at Carnegie stages 22 and 23. This is the first description of the caudal portion of the fused Müllerian ducts separating again and returning to each of the Wolffian ducts in human embryos. Copyright 2003 Wiley-Liss, Inc.

PMID: 12740945

MicroRNA in the ovary and female reproductive tract

Carletti MZ, Christenson LK. J Anim Sci. 2009 Apr;87(14 Suppl):E29-38. Epub 2008 Sep 12. Review. PMID: 18791135

"Interestingly, when Dicer1 expression is decreased in reproductive tissues or cells, the females are infertile."

Meeting report: measuring endocrine-sensitive endpoints within the first years of life. Arbuckle TE, Hauser R, Swan SH, Mao CS, Longnecker MP, Main KM, Whyatt RM, Mendola P, Legrand M, Rovet J, Till C, Wade M, Jarrell J, Matthews S, Van Vliet G, Bornehag CG, Mieusset R. Environ Health Perspect. 2008 Jul;116(7):948-51. PMID: 18629319 | PMC: 2453165] | Supplementary PDF

"An international workshop titled "Assessing Endocrine-Related Endpoints within the First Years of Life" was held 30 April-1 May 2007, in Ottawa, Ontario, Canada. Representatives from a number of pregnancy cohort studies in North America and Europe presented options for measuring various endocrine-sensitive endpoints in early life and discussed issues related to performing and using those measures. The workshop focused on measuring reproductive tract developmental endpoints [e.g., anogenital distance (AGD)], endocrine status, and infant anthropometry. To the extent possible, workshop participants strove to develop or recommend standardized measurements that would allow comparisons and pooling of data across studies. The recommended outcomes include thigh fat fold, breast size, vaginal cytology, AGD, location of the testis, testicular size, and growth of the penis, with most of the discussion focusing on the genital exam. Although a number of outcome measures recommended during the genital exam have been associated with exposure to endocrine-disrupting chemicals, little is known about how predictive these effects are of later reproductive health or other chronic health conditions."

Anogenital distance from birth to 2 years: a population study

Environ Health Perspect. 2009 Nov;117(11):1786-90. Epub 2009 Jul 13.

Thankamony A, Ong KK, Dunger DB, Acerini CL, Hughes IA.

Department of Paediatrics, University of Cambridge, Cambridge, United Kingdom. Abstract BACKGROUND: Anogenital distance (AGD) is sexually dimorphic in rodents and humans, being 2- to 2.5-fold greater in males. It is a reliable marker of androgen and antiandrogen effects in rodent reproductive toxicologic studies. Data on AGD in humans are sparse, with no longitudinal data collected during infancy.

OBJECTIVE: This study was designed to determine AGD from birth to 2 years in males and females and relate this to other anthropometric measures.

MATERIALS AND METHODS: Infants were recruited from the Cambridge Baby Growth Study. AGD was measured from the center of the anus to the base of the scrotum in males and to the posterior fourchette in females. Measurements were performed at birth and at 3, 12, 18, and 24 months of age.

RESULTS: Data included 2,168 longitudinal AGD measurements from 463 male and 426 female full-term infants (median = 2 measurements per infant). Mean AGD (+/- SD) at birth was 19.8 +/- 6.1 mm in males and 9.1 +/- 2.8 mm in females (p < 0.0001). AGD increased up to 12 months in both sexes and in a sex-dimorphic pattern. AGD was positively correlated with penile length at birth (r = 0.18, p = 0.003) and the increase in AGD from birth to 3 months was correlated with penile growth (r = 0.20, p = 0.001).

CONCLUSION: We report novel, longitudinal data for AGD during infancy in a large U.K. birth cohort. AGD was sex dimorphic at all ages studied. The availability of normative data provides a means of utilizing this biological marker of androgen action in population studies of the effects of environmental chemicals on genital development.

PMID: 20049133

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801188/?tool=pubmed