» > Its known that the variant of the androgen receptor gene is located on
» > x-chromosome and comes from your mother, but the other genes in
» An ectodysplasin gene (which is located on the X chromosome, near the AR
» gene) has now been linked to MPB. The ectodysplasin signalling system has
» already been shown to be important in hair biology…do a search on Pubmed
» for more details. You’ll be hearing about this study in the lay media
» pretty soon, I’m sure:
» J Invest Dermatol. 2008 Apr 3 [Epub ahead of print]
» EDA2R Is Associated with Androgenetic Alopecia.
» Prodi DA, Pirastu N, Maninchedda G, Sassu A, Picciau A, Palmas MA, Mossa
» A, Persico I, Adamo M, Angius A, Pirastu M.
» 1Shardna Life Sciences, Pula, Italy.
» Androgenetic alopecia (AGA) is a common heritable polygenic disorder whose
» genetics is not fully understood, even though it seems to be X-linked. We
» carried out an epidemiological survey for AGA on 9,000 people from 8
» isolated villages of a secluded region of Sardinia (Ogliastra), and
» identified a large cohort of affected individuals. We genotyped 200 cases
» and 200 controls (mean kinship 0.001) with the 500k chip array and
» conducted case-control association analysis on the X chromosome. We
» identified Xq11-q12 as strongly associated with AGA. In particular, we
» found that rs1352015 located 8 kb from the EDA2R gene showed the best
» result (P=7.77e(-7)). This region also contains the AR gene, hence we
» tested both genes in 492 cases and 492 controls. We found that the
» non-synonymous SNP rs1385699 on EDA2R gave the best result (P=3.9e(-19))
» whereas rs6152 on the AR gene is less significant (P=4.17e(-12)). Further
» statistical analysis carried out by conditioning each gene to the presence
» of the other showed that the association with EDA2R is independent while
» the association with AR seems to be the result of linkage disequilibrium.
» These results give insight into the pathways involved in AGA etiology.
» Journal of Investigative Dermatology advance online publication, 3 April
» PMID: 18385763 [PubMed - as supplied by publisher]
That link you posted, showing a gene that is statsitically signifigant in baldness, and almost assuredly has a direct influence on it, got me to looking around and I came up with this…
Min Zhang 1, Anna Brancaccio 2, Lorin Weiner 1, Caterina Ectodysplasin regulates pattern formation in the mammalian hair coat Missero 2, Janice L. Brissette 1 *
1Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, USA
2Telethon Institute of Genetics and Medicine (TIGEM), Naples, Italy
email: Janice L. Brissette (email@example.com)
*Correspondence to Janice L. Brissette, Cutaneous Biology Research Center, Massachusetts General Hospital-East, Bldg. 149, 13th St., Charlestown, MA 02129
National Institutes of Health
Cutaneous Biology Research Center through the Massachusetts General Hospital/Shiseido Co. Ltd. Agreement
Italian Telethon Foundation
TIGEM with funding from Regione Campania
Eda • tabby • ectodermal dysplasia • ED1 • Edar
Summary: develoIn mammalian skin, hair follicles develop at regular intervals and with site-specific morphologies. This process generates distinct patterns of hair, but the mechanisms that establish these patterns remain largely unknown. Here we present evidence of follicular patterning by ectodysplasin-A1 (Eda-A1), a signaling protein necessary for the proper development of hair and other appendages. In transgenic mice, Eda-A1 was targeted to the epithelial compartment of the ping skin. At periodic locations, multiple hair follicles were induced side by side, without any interfollicular space. These follicles grew into the dermis as a fusion and subsequently branched to create discrete stalks and hair bulbs. Thus, at sites where interfollicular skin normally forms, hair follicles developed instead. This result shows that Eda-A1 can regulate basic developmental decisions, as cells were switched from interfollicular to follicular fates. Given these effects, it is likely that Eda-A1 is among the key regulators of pattern formation in the skin. genesis 37:30-37, 2003. © 2003 Wiley-Liss, Inc.
Me again…perhaps this ‘Ectodermal-A1’ gene is the one that makes the decisions as your head skin grows up over your head in fetal development and determines where your most androgen-sensitive hair will be (the shape of your hippocratic wreath), or where your best working androgen-receptors will be (Im basing this on a study I saw that showed androgen receptors in sebaceous glands in male pattern baldness subjects were much better at uptaking androgens that receptors from sweat glands from occipital scalp). A working “guess” is forming anyway in my mind about it. Here is another study showing that ectodysplasin ‘gene’ and the development of the sweat glands (Do you remember how Stephen Foote used to go on about how bald areas of scalp are better at sweating than hairy areas of scalp? Maybe this is a reason why----other than the sweat glands in bald scalp receptor-sites probably have more available testosterone around due to the tiny vellus hairs not having as many androgen receptors available to uptake androgen in a competing sense physically:
[Relationship of ectodysplasin gene signaling with development and regeneration of sweat glands][Article in Chinese]
Zhou G, Li H, Fu X.
Key Research Laboratory of the Wound Repair, the 304th Clinical Department, General Hospital of PLA, Beijing, 100037, P.R. China.
OBJECTIVE: To investigate the expression of ectodysplasin (EDA) gene signaling and its relationship with the development and regeneration of sweat glands. METHODS: The articles concerned in the latest years were extensively reviewed. RESULTS: EDA gene is an important signaling pathway associated with the developmental procedure of sweat glands in early fetal stage. Abnormality or depletion of function in sweat glands partially owed to the defect of EDA gene. CONCLUSION: EDA signaling has its biological significance in inducing development and morphogenesis of sweat glands and in maintaining physiological function of skin. It could be a new approach to repair or regenerate the sweat glands for clinical therapy by regulating the expression of EDA gene.
PMID: 16752854 [PubMed - in process]
Me again (again–LOL)…TAGOHL, I know the sweat glands would at first seem to be unimportant, but they are tissues in the dermis and here we have that same gene again seemingly being involved on an important part of the skin. Loren Pickart has wrote on his site that the hair follicle seems to be the “command center” for skin-remodelling and signalling. I always noticed that women who pluck out their moustaches repeatedly after menopause seemingly have the upper portions of their mouths age terribly after the hair follicles get destroyed from repeatedly pulling them out-----