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2009/12/03 01:38:06瀏覽64|回應0|推薦0 | |
今天在Yahoo新聞中看到一篇很有趣的科技新聞「短命基因 來自父系遺傳」,內容提到東京農業大學科學家製造出無父偶母的母鼠BM(Bi-maternal Mice),不是精蟲與卵子的結合,而是卵子與卵子的結合,"生"下來的老鼠簡稱BM,都是母的,體形較小。BM相較於對照組(Control mice),平均壽命多出186天。無父偶母的母鼠壽命要比一般老鼠多出三分之一。BM長壽可能反映其基因體印記(imprinted)的方式不正常,因為牠們沒有父系的DNA。 我搜尋了一下網路,原文中有一段標題為Reduced body size and increased blood eosinophil count in the BM,雖是就實驗結果來做推論,似乎將長壽歸功於較小的體形及較多的嗜伊紅血球(eosinophil)。利用精子繁殖出來的母鼠,會帶有從父鼠那邊過來的Rasgrf1 (a paternally methylated imprinted gene on chromosome 9 associated),擁有DM所沒有的 --- 增加體重的印記(imprinted)。體型可能與長壽有很大的關係,減重不見得可以延壽,但現在的普遍認知是:飲食控制,而非營養失調及降低代謝率,真的會延壽。嗜伊紅血球的作用我不是很了解,它是與發炎反應、免疫系統有關的。 實驗設計的很有趣,會有人想出這種實驗,我看到的第一個反應是新奇有趣,大開眼戒。(對不起,鼠輩們,你們又受苦了。)實驗者認為既然雌向來比雄長壽,想研究看看無精蟲繁殖出來的母鼠會怎樣? 第二就是一個疑問:人活這麼久是要幹嘛? 除非活得久,有一些生存智慧及經驗會成為印記基因的一部份,繁衍給下一代,讓下一代更加適者生存、生存者適。不過老者無法繁殖,更具生存經驗與智慧的印記基因傳得下去得靠生物科技。人活得久是自然法則還是不是自然法則?不是自然法則的東西可無法 last long。
我的第三個反應是:從很多形而上、形而下的理論,顯示出一陰一陽是不變的道理。世界上若全是雄性會是個大災難,若全是雌性呢?實驗者設計者的原本想證明的,會不會是:就算是雌比雄長壽,無父偶母的可是會活不久的?記得看過英國當年發展桃莉羊的書,實驗室裡合成的牛羊胚胎不知道為什麼都活不久。
看來BM結果相反。如果沒有男性,女性一樣可以繁殖得很好且活得更久的話,男性可要跳腳了。
這一篇原文名為Longevity in mice without a father,刊登於Human Reproduction,12月1日才發表的,內容很新,謹摘要部份內容如下:
BACKGROUND: Females live longer than males in many mammalian species, including humans. It has been observed that women are at an advantage over men with regard to the lifespan; however, the reason for this sex difference in longevity is unclear. Bi-maternal mice (BM), which are produced in a ‘sperm-free’ manner, could provide an opportunity to analyse the longevity of animals lacking paternal genomes.
METHODS AND RESULTS: We studied the longevity of BM, which were generated using two sets of female genomes—one derived from fully grown oocytes from normal adults and the other from non-growing oocytes from newborn pups. These newborn pups were also genetically manipulated in two regions—the imprinting centres of Igf2-H19 and Dlk1-Gtl2—on chromosomes 7 and 12. We determined lifespan of the control (n = 13) and BM (n = 13). Our results revealed that the bi-maternal genotype clearly shifted the entire survival curve to the right, suggesting a delay in the expression of all causes of mortality. BM survived 186 days longer than controls. Furthermore, the body weight was significantly lower in the BM as compared with the controls at 20 months after birth (P < 0.05), and leukocyte composition analysis at 8 weeks revealed that the eosinophil count was significantly increased in the BM as compared with the controls (P < 0.05, n = 6).
CONCLUSIONS: These findings demonstrate that the maternal genome may play a role in ontogenetic longevity. Our results further suggested sex differences in longevity, originating at the genome level, implying that the sperm genome has a detrimental effect on longevity in mammals.
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