近日,，韓國的科學(xué)家發(fā)現(xiàn),，在胚胎期敲除雌性老鼠的一個單基因，可使雌性老鼠變成“同性戀”,。
這個簡易的手術(shù)使得基因被敲除的雌性老鼠拒絕雄性老鼠的求愛行為,，同時試圖與其雌性同類進(jìn)行交配。研究者發(fā)現(xiàn),，敲除FucM基因（該基因影響了雌激素的水平,，進(jìn)而使大腦受到影響）使得雌性老鼠在長大過程中的行為與雄性接近。
韓國科學(xué)技術(shù)院的帕克教授（Chankyu Park）領(lǐng)導(dǎo)了這項(xiàng)研究,。他說：“基因被改造的雌性老鼠的大腦發(fā)展軌跡被改變,，使其在性取向方面接近雄性同類。”其實(shí),，全球科學(xué)家在尋找“同性戀與基因”之間的關(guān)聯(lián)已有相當(dāng)長的時間,，但是進(jìn)行這項(xiàng)最新研究的學(xué)者強(qiáng)調(diào)稱，目前該試驗(yàn)這還無法表明是否與人類的性活動存在某種相關(guān)性,。
通過敲除這種特殊基因,，科學(xué)家認(rèn)為他們可以通過阻止雌性老鼠大腦過濾掉性激素，使雌性老鼠受到額外雌激素影響,。雖然雌激素（的變化）能使雌性老鼠的大腦雄性化,，但是在人類中并未發(fā)現(xiàn)相同的效應(yīng)。
帕克教授接下來將考察該基因產(chǎn)生的酶（一種海藻糖變旋酶）是否對人類性活動具有影響,，不過他承認(rèn)想找到愿意參與實(shí)驗(yàn)的自愿者可能“十分困難”,。他的大部分研究都已經(jīng)發(fā)表在《英國醫(yī)學(xué)委員會遺傳學(xué)》（BMC Genetics）雜志上。(生物谷Bioon.net)
生物谷推薦原文出處：
BMC Genetics. PMID: 20609214
Male-like sexual behavior of female mouse lacking fucose mutarotase.
Park D, Choi D, Lee J, Lim DS, Park C.
ABSTRACT: BACKGROUND: Mutarotases are recently characterized family of enzymes that are involved in the anomeric conversions of monosaccharides. The mammalian fucose mutarotase (FucM) was reported in cultured cells to facilitate fucose utilization and incorporation into protein by glycosylation. However, the role of this enzyme in animal has not been elucidated. RESULTS: We generated a mutant mouse specifically lacking the fucose mutarotase (FucM) gene. The FucM knockout mice displayed an abnormal sexual receptivity with a drastic reduction in lordosis score, although the animals were fertile due to a rare and forced intromission by a typical male. We examined the anteroventral periventricular nucleus (AVPv) of the preoptic region in brain and found that the mutant females showed a reduction in tyrosine hydoxylase positive neurons compared to that of a normal female. Furthermore, the mutant females exhibited a masculine behavior, such as mounting to a normal female partner as well as showing a preference to female urine. We found a reduction of fucosylated serum alpha-fetoprotein (AFP) in a mutant embryo relative to that of a wild-type embryo.
CONCLUSIONS: The observation that FucM-/- female mouse exhibits a phenotypic similarity to a wild-type male in terms of its sexual behavior appears to be due to the neurodevelopmental changes in preoptic area of mutant brain resembling a wild-type male. Since the previous studies indicate that AFP plays a role in titrating estradiol that are required to consolidate sexual preference of female mice, we speculate that the reduced level of AFP in FucM-/- mouse, presumably resulting from the reduced fucosylation, is responsible for the male-like sexual behavior observed in the FucM knock-out mouse.
