HOX genes encode transcription factors that help determine the body plan—including the positional identity of the female reproductive tract—during development. They also control the development and receptivity of the endometrium
2015 Study Abstract
HOX genes convey positional identity that leads to the proper partitioning and adult identity of the female reproductive track.
Abnormalities in reproductive tract development can be caused by HOX gene mutations or altered HOX gene expression. Diethylstilbestrol (DES) and other endocrine disruptors cause Müllerian defects by changing HOX gene expression.
HOX genes are also essential regulators of adult endometrial development. Regulated HOXA10 and HOXA11 expression is necessary for endometrial receptivity; decreased HOXA10 or HOXA11 expression leads to decreased implantation rates. Alternation of HOXA10 and HOXA11 expression has been identified as a mechanism of the decreased implantation associated with endometriosis, polycystic ovarian syndrome, leiomyoma, polyps, adenomyosis, and hydrosalpinx.
Alteration of HOX gene expression causes both uterine developmental abnormalities and impaired adult endometrial development that prevent implantation and lead to female infertility.
Sources and more information
- The Role of Hox Genes in Female Reproductive Tract Development, Adult Function, and Fertility, Cold Spring Harbor perspectives in medicine, NCBI PubMed PMID: 26552702, 2015 Nov.
- Hands featured image credit Andrew Storms.
DES DIETHYLSTILBESTROL RESOURCES
- Source DES and epigenetics studies.
- Diethylstilbestrol DES studies by topics.