在1月23日的《科学》杂志中,科学家们在2篇互为参证的研究中说,地区性的语言和胃里的细菌都告诉了我们人类是如何从亚洲迁徙出来并在整个太平洋中散布开来的。
该图显示了幽门螺旋杆菌在亚洲和太平洋地区的分布。(来源:《科学》)
研究人员长期以来都对人群是如何在太平洋上各地区定居的感到兴趣,包括人们是如何在许多地处偏远且与外界隔离的岛屿上定居的。Colin Renfrew在一篇讨论这2篇文章的Perspective中,对这一问题进行了解释。Yoshan Moodley及其同僚对这一问题采用了一种新的研究方法,他们对台湾和澳大利亚的土著人、新几内亚高地人以及居住在新喀里多尼亚的美拉尼西亚和波利尼西亚人体内的幽门弯曲菌(Helicobacter pylori)进行了采样。在那些无法获取现代医药的人群中,大约有一半的人的胃中有幽门弯曲菌。由于这种细菌是人特有的,因此它随着其宿主在世界上传播,而且随着宿主而发生遗传上的歧化。Moodley及其同僚对他们的细菌样本的DNA序列进行了比较并发现了2个菌株,这两个菌株看来已经分别演化达数千年之久。其中一个菌株(他们称为hpSahul)在3万年前就与亚洲人的幽门弯曲菌分道扬镳,这可能与人们跨越暴露的大陆桥(即现在的印度尼西亚群岛)进入新几内亚和澳大利亚有关。另外一个菌株(hpMaori)是在大约5000年前从台湾播散出去的,当时第二波的人潮迁徙到了菲律宾并进入波利尼西亚和新西兰。
R.D. Gray及其同僚在他们对南岛语言的比较中对这一第二波的迁徙进行了更为详尽的分析。他们基于跨越一整套内有210个核心词汇的字的语言的相似性(或称“同源性”)构建了一颗演化树,从中显示了400种语言之间的关系。结果表明,南岛语系植根于台湾,并在大约5000年前开始多元化。人口的迁徙也包括2次主要的停顿,第一次停顿发生在人们定居在台湾和定居在菲律宾的时期之间(造成这一停顿的原因可能是人们在跨越隔开两者的长达350英里的海峡时遭遇困难);第二次的停顿发生在西波利尼西亚(造成这一停顿的原因或许是人们在应付与东波利尼西亚的岛屿之间的辽阔的距离时必须要有更进一步的技术和/或社会的创新)。(生物谷Bioon.com)
生物谷推荐原始出处:
Science 23 January 2009: Vol. 323. no. 5913, pp. 530 - 533 DOI: 10.1126/science.1165740
Rapid Membrane Disruption by a Perforin-Like Protein Facilitates Parasite Exit from Host Cells
Bj?rn F. C. Kafsack,1,2 Janethe D. O. Pena,3 Isabelle Coppens,2 Sandeep Ravindran,4 John C. Boothroyd,4 Vern B. Carruthers1*
Perforin-like proteins are expressed by many bacterial and protozoan pathogens, yet little is known about their function or mode of action. Here, we describe Toxoplasma perforin-like protein 1 (TgPLP1), a secreted perforin-like protein of the intracellular protozoan pathogen Toxoplasma gondii that displays structural features necessary for pore formation. After intracellular growth, TgPLP1-deficient parasites failed to exit normally, resulting in entrapment within host cells. We show that this defect is due to an inability to rapidly permeabilize the parasitophorous vacuole membrane and host plasma membrane during exit. TgPLP1 ablation had little effect on growth in culture but resulted in a reduction greater than five orders of magnitude of acute virulence in mice. Perforin-like proteins from other intracellular pathogens may play a similar role in microbial egress and virulence.
1 Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
2 Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
3 Department of Immunology, Universidade Federal de Uberlandia, Uberlandia, Brazil.
4 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.