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“Epigenetics” proposed to underlie homosexuality

Dec. 12, 2012
Courtesy of National Institute for 
Mathematical and Biological Synthesis
and World Science staff

A key fac­tor be­hind ho­mo­sex­u­al­ity may be not ge­net­ics, but epige­net­ics—the way tem­po­rary “switch­es” in our cells in­flu­ence gene ac­ti­vity, sci­en­tists are re­port­ing.

New re­search sug­gests ho­mo­sex­u­al­ity can oc­cur when sex-spe­cif­ic forms of these switch­es—nor­mally “erased” be­tween genera­t­ion­s—escape eras­ure. Thus, a switch is passed from fa­ther to daugh­ter or from moth­er to son, along with traits more typ­i­cal of the op­po­site sex.

This graph­ic il­lus­trates how traits are af­fect­ed by ep­i­ge­net­ic mech­a­nisms. A key step is DNA meth­yl­a­tion, in which a mol­e­cule called a me­thyl group at­taches it­self to the DNA and there­by ac­ti­vates or re­presses genes. The meth­yl­a­tion af­fects the way DNA is "wrapped up" around struc­tures called hi­s­tones, which look like yo-yos. This wrap­ping causes genes in the wrapped-up sec­tion of DNA to be re­pressed be­cause they're in­ac­ces­si­ble to oth­er cel­lu­lar mech­a­nisms. (Im­age cour­te­sy U.S. Nat'l Can­cer In­sti­tute)


The re­search­ers de­vised a mathematical-biological mod­el point­ing to the epige­net­ics con­nec­tion; and though it re­mains un­prov­en, they said it solves a key rid­dle.

Why ho­mo­sex­u­al­ity is com­mon is a ques­tion that has per­plexed bi­ol­o­gists. Dar­win­i­an the­o­ry sug­gests that over genera­t­ions, same-sex ori­enta­t­ion would tend to elim­i­nate it­self from a popula­t­ion, since pure ho­mo­sex­u­als pre­sumably don’t re­pro­duce. Stud­ies have none­the­less found same-sex pref­er­ence runs in fam­i­lies, lead­ing most re­search­ers to pre­sume there must be a gene for it, though it has not clearly turned up.

In the new work, re­search­ers de­vised a biological-mathematical mod­el de­fin­ing the role of epige­net­ics in ho­mo­sex­u­al­ity, by in­te­grat­ing ev­o­lu­tion­ary the­o­ry with ad­vanc­es in the mo­lec­u­lar con­trol of gene ac­ti­vity and hormone-dependent sex­u­al de­vel­op­ment. 

The find­ings are pub­lished on­line Dec. 11 in The Quar­terly Re­view of Bi­ol­o­gy.

Epi-marks con­sti­tute an ex­tra lay­er of in­forma­t­ion at­tached to our genes’ back­bones that reg­u­lates their ex­pres­sion, ex­plained the au­thors, based at the the Na­t­ional In­sti­tute for Math­e­mat­i­cal and Bi­o­log­i­cal Syn­the­sis in Knox­ville, Tenn. While genes hold the in­struc­tions, epi-marks di­rect how those in­struc­tions are car­ried out – when, where and how much a gene is ac­tivated dur­ing de­vel­op­ment. By the ac­tiva­t­ion of a gene, or its “ex­pres­sion,” sci­en­tists mean that the gene is pro­duc­ing a pro­tein spe­cif­ic to that gene, and which car­ries out spe­cif­ic func­tions.

Epi-marks are usu­ally pro­duced anew each genera­t­ion, but re­cent stud­ies in­di­cate that they some­times car­ry over be­tween genera­t­ions, lead­ing to an ef­fect that re­sem­bles shared genes.

Sex-spe­cif­ic epi-marks pro­duced in early de­vel­op­ment pro­tect each sex from the nat­u­ral varia­t­ion in tes­tos­ter­one that oc­curs dur­ing fe­tal de­vel­op­ment, the au­thors of the new study not­ed. Epi-marks stop girl fe­tus­es from be­ing “mas­culin­ized” when they ex­pe­ri­ence very high tes­tos­ter­one, and vi­ce versa for boys.

Dif­fer­ent epi-marks pro­tect dif­fer­ent sex-spe­cif­ic traits from be­ing mas­cu­lin­ized or fem­i­nized – some af­fect the gen­i­tals, oth­ers sex­u­al ident­ity, and yet oth­ers af­fect sex­u­al part­ner pref­er­ence. When these epi-marks are trans­mit­ted across genera­t­ions from fa­thers to daugh­ters or moth­ers to sons, they pre­sumably cause re­versed ef­fects, such as the femin­iz­a­tion of some traits in sons, such as sex­u­al pref­er­ence, and a par­tial mas­culin­iz­a­tion of daugh­ters.

This un­usu­al pro­cess is termed the “trans­mis­sion of sex­u­ally an­tag­o­nis­t epi-marks,” ex­plained the stu­dy’s co-author, Sergey Gavrilets of the in­sti­tute. It’s “the most plau­si­ble ev­o­lu­tion­ary mech­an­ism of the phe­nom­e­non of hu­man ho­mo­sex­u­al­ity,” he added. And it does­n’t suf­fer from con­tra­dic­tions with ev­o­lu­tion­ary the­o­ry, he ar­gued: un­like a “ho­mo­sex­u­al­ity gene,” genes pro­duc­ing these epi-marks can easily spread in popula­t­ions, since they’re fa­vor­a­ble to reproduction—u­su­ally.


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A key factor behind homosexuality may be not genetics, but epigenetics—the way temporary “switches” in our cells govern gene activity, scientists are reporting. New research suggests homosexuality can occur when sex-specific forms of these switches—normally “erased” between generations—escape erasure. Thus, a switch is passed from father to daughter or from mother to son, along with traits more typical of the opposite sex. The researchers devised a mathematical-biological model pointing to the epigenetics connection; and though it remains unproven, they said it solves a key riddle. Why homosexuality is common is a question that has perplexed biologists. Darwinian theory suggests that over generations, same-sex orientation would tend to eliminate itself from a population, since pure homosexuals presumably don’t reproduce. Studies have nonetheless found same-sex preference runs in families, leading most researchers to presume there must be a gene for it, though it has not clearly turned up. In the new work, researchers devised a biological-mathematical model defining the role of epigenetics in homosexuality, by integrating evolutionary theory with advances in the molecular control of gene activity and hormone-dependent sexual development. The findings are published online Dec. 11 in The Quarterly Review of Biology. Epi-marks constitute an extra layer of information attached to our genes’ backbones that regulates their expression, explained the authors, based at the the National Institute for Mathematical and Biological Synthesis in Knoxville, Tenn. While genes hold the instructions, epi-marks direct how those instructions are carried out – when, where and how much a gene is activated during development. By the activation of a gene, or its “expression,” scientists mean that the gene is producing a protein specific to that gene, and which carries out specific functions. Epi-marks are usually produced anew each generation, but recent studies indicate that they sometimes carry over between generations, leading to an effect that resembles shared genes. Sex-specific epi-marks produced in early development protect each sex from the natural variation in testosterone that occurs during fetal development, the authors of the new study noted. The epi-marks stop girl fetuses from being “masculinized” when they experience atypically high testosterone, and vice versa for boys. Different epi-marks protect different sex-specific traits from being masculinized or feminized – some affect the genitals, others sexual identity, and yet others affect sexual partner preference. When these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they presumably cause reversed effects, such as the feminization of some traits in sons, such as sexual preference, and a partial masculinization of daughters. This unusual process is termed the “transmission of sexually antagonistic epi-marks,” explained the study’s co-author, Sergey Gavrilets of the institute. It’s “the most plausible evolutionary mechanism of the phenomenon of human homosexuality,” he added. And it doesn’t suffer from contradictions with evolutionary theory, he argued: unlike a “homosexuality gene,” genes producing these epi-marks can easily spread in populations, since they’re favorable to reproduction—usually.