近日,，麻省理工大學(xué)E. Alm領(lǐng)導(dǎo)的研究組發(fā)現(xiàn),，全世界2,235組細(xì)菌基因組中的10,000個(gè)基因,，正以"水平基因轉(zhuǎn)移(HGT)"的方式自由流動(dòng)。這說明所有細(xì)菌在一個(gè)由全世界細(xì)菌基因組組成的大網(wǎng)絡(luò)上頻繁地交換著遺傳物質(zhì),。這一研究成果發(fā)表在10月30號(hào)的網(wǎng)絡(luò)版雜志《自然》上,。
科學(xué)家很早就知道HGT，它是細(xì)菌的一種很古老的行為--來自不同支系的細(xì)菌通過交換,，獲得從父母那里得不到的遺傳信息,。如果交換到的基因能使細(xì)菌具備有用的特征，則這一基因受到正選擇會(huì)傳遞給它的后代,。但到底交換了多少信息，速度有多快,？該研究組的工作表明基因隨著細(xì)菌繁殖以相當(dāng)大的范圍和速度在擴(kuò)散,。
有時(shí)候這對(duì)人類構(gòu)成威脅，比如獲得抗藥性基因的細(xì)菌（"超級(jí)細(xì)菌(superbugs)"）,。他們此次發(fā)現(xiàn)了一個(gè)抗藥性的基因出現(xiàn)在人類共生菌的六成的基因轉(zhuǎn)移中,。這種抗藥性基因可能是在工業(yè)化農(nóng)業(yè)的抗生素濫用中產(chǎn)生的。牲畜共生菌和人類共生菌中有42個(gè)相同的抗藥性基因,，也就是說這兩類細(xì)菌共享一個(gè)基因庫,，盡管10億年的進(jìn)化早該讓牛身上的細(xì)菌和人身上的細(xì)菌分道揚(yáng)鑣。向動(dòng)物的食物中加入預(yù)防疾病的抗生素,，可以促進(jìn)其生長(zhǎng),，防止高密度養(yǎng)殖的牲畜和家禽內(nèi)部的疾病傳播。雖然許多歐洲國(guó)家已經(jīng)明令禁止,，但在美國(guó)還很普遍,。根據(jù)聯(lián)邦藥物管理局（the Federal Drug Administration）的報(bào)告,，2009年在美國(guó)銷售的3.3千萬磅抗生素中80%用于農(nóng)業(yè)，里面就包括通常作為人類藥物的青霉素,，四環(huán)素,。
另外還發(fā)現(xiàn)了抗藥性基因跨國(guó)轉(zhuǎn)移的43個(gè)例子。這說明,，一旦一個(gè)基因攜帶某個(gè)特征進(jìn)入人類共生菌的基因庫,，很快它就會(huì)傳播到國(guó)界之外，成為一個(gè)嚴(yán)重國(guó)際性問題,。
Alm的研究組還發(fā)現(xiàn),，同一寄主的細(xì)菌之間，HGT發(fā)生更頻繁,。具有相同的氧氣耐受力或相同的致病性,，使它們占據(jù)相同的環(huán)境生態(tài)位，這比親緣關(guān)系相近或地理位置相近更能決定一個(gè)轉(zhuǎn)移基因是否能融入新的細(xì)菌基因組中,。 研究組根據(jù)這個(gè)準(zhǔn)則尋找能引起腦膜炎和其他疾病的基因,，希望發(fā)現(xiàn)轉(zhuǎn)移和編碼這些特征的基因，未來藥物治療可能將以此為靶向,。
美國(guó)科羅拉多大學(xué)的R. Knight說,，"這是一項(xiàng)有趣的工作，完整基因組序列的數(shù)據(jù)庫不斷擴(kuò)大,，再配合大量細(xì)致的環(huán)境特征數(shù)據(jù),，就可能發(fā)現(xiàn)大尺度的進(jìn)化模式，那時(shí)我們就能以前所未有的視角來統(tǒng)觀地球上的所有微生物,。"
研究組還在繼續(xù)這項(xiàng)研究,，現(xiàn)在正在比對(duì)在同一寄主身上不同細(xì)菌間，和相同疾病,、不同寄主的細(xì)菌間的交換速度有什么差異,。他們也考察環(huán)境污染地區(qū)細(xì)菌的基因交換，期待那里有能消化重金屬的細(xì)菌,。（生物谷 Bioon.com）
doi:10.1038/nature1057
PMC:
PMID:
Ecology drives a global network of gene exchange connecting the human microbiome
Chris S. Smillie, Mark B. Smith, Jonathan Friedman, Otto X. Cordero, Lawrence A. David& Eric J. Alm
Horizontal gene transfer (HGT), the acquisition of genetic material from non-parental lineages, is known to be important in bacterial evolution. In particular, HGT provides rapid access to genetic innovations, allowing traits such as virulence, antibiotic resistance and xenobiotic metabolism to spread through the human microbiome. Recent anecdotal studies providing snapshots of active gene flow on the human body have highlighted the need to determine the frequency of such recent transfers and the forces that govern these events. Here we report the discovery and characterization of a vast, human-associated network of gene exchange, large enough to directly compare the principal forces shaping HGT. We show that this network of 10,770 unique, recently transferred (more than 99% nucleotide identity) genes found in 2,235 full bacterial genomes, is shaped principally by ecology rather than geography or phylogeny, with most gene exchange occurring between isolates from ecologically similar, but geographically separated, environments. For example, we observe 25-fold more HGT between human-associated bacteria than among ecologically diverse non-human isolates (P = 3.0?×?10(-270)). We show that within the human microbiome this ecological architecture continues across multiple spatial scales, functional classes and ecological niches with transfer further enriched among bacteria that inhabit the same body site, have the same oxygen tolerance or have the same ability to cause disease. This structure offers a window into the molecular traits that define ecological niches, insight that we use to uncover sources of antibiotic resistance and identify genes associated with the pathology of meningitis and other diseases.
