為什么進(jìn)化的速度以及復(fù)雜性變得越來越快,?根據(jù)化石記錄顯示,,單細(xì)胞生物于35億年前首次出現(xiàn)在地球上,但是之后它們用了大約25億年進(jìn)化成多細(xì)胞生物,,剩下的10億年卻發(fā)展成了植物,、哺乳動(dòng)物、昆蟲,、鳥類等各種各樣的地球物種,。
Rice大學(xué)科學(xué)家的研究結(jié)果可望解決這一問題,他們認(rèn)為生物進(jìn)化速度的加快是因?yàn)榧?xì)菌和病毒不斷在不同物種之間傳遞DNA,,如果沒有這種作用,,只依靠基因突變和兩性選擇作用是不會(huì)達(dá)到如此快速度的。
Rice大學(xué)的Michael Deem說:“我們創(chuàng)造了第一個(gè)能解釋物種間基因交換的進(jìn)化數(shù)學(xué)模型,。”結(jié)果發(fā)表在了1月29日的《Physical Review Letters》上,。過去的數(shù)學(xué)模型主要關(guān)注生物如何對(duì)點(diǎn)突變做出反應(yīng),很少的理論關(guān)注再結(jié)合過程,。
基因水平轉(zhuǎn)移(HGT)是物種間的基因轉(zhuǎn)移,,是DNA從一個(gè)物種轉(zhuǎn)移另一個(gè)物種。在50年前這一想法首次被提出時(shí)受到科學(xué)家的嘲笑,,但是細(xì)菌抗藥性的出現(xiàn)以及其它的很多發(fā)現(xiàn),,包括細(xì)菌用來交換基因的特定蛋白使這一理論在最近逐漸被接受。
Deem說:“我們知道動(dòng)植物的很多DNA來自HGT過程,,包括人類。”這一由Deem和Jeong-Man Park創(chuàng)造的新型模型用來解釋HGT過程對(duì)于進(jìn)化動(dòng)力學(xué)的影響,。過去的模型只能解釋點(diǎn)變異,,Deem和Park的模型顯示了HGT如何通過傳遞變異增加進(jìn)化的速度,。
在一月的《Physics Today》上,Deem就描述了HGT的重要性,,例如幫助細(xì)菌擁有對(duì)抗抗生素的抗藥性等,。
部分英文原文:
A Physical Theory of the Competition that Allows HIV to Escape from the Immune System
Guanyu Wang1,2 and Michael W. Deem1
1Department of Bioengineering and Department of Physics & Astronomy,
Rice University, Houston, TX 77005–1892, USA
2Department of Physics, George Washington University, Washington, D.C. 20052, USA
Competition within the immune system may degrade immune control of viral infections. We
formalize the evolution that occurs in both HIV-1 and the immune system quasispecies. Inclusion
of competition in the immune system leads to a novel balance between the immune response and
HIV-1, in which the eventual outcome is HIV-1 escape rather than control. The analytical model
reproduces the three stages of HIV-1 infection. We propose a vaccine regimen that may be able to
reduce competition between T cells, potentially eliminating the third stage of HIV-1.
Our immune system is highly effective in suppressingmost viral infections, due to the many different T cells that exist in the repertoire of one person. While many different T cells can recognize a virus, only those of highest affinity respond in large numbers and participate in eliminating the virus. One limitation of our immune system stems from the competition among T cells of similar specificity for the virus. For a series of discrete infections over time, competition in the immune system is associated with the phenomenon of deceptive imprinting [1], or original antigenic sin, and has been characterized by a random energy model [2]. Original antigenic sin is the tendency for memory immune cells produced in response to a first viral infection to suppress the creation of new immune cells in response to a second infection with a related strain. Moreover, while they are used, these memory immune cells may not be optimal for control of this second, different viral strain. Another form of competition in the immune system occurs when several viral strains simultaneously infect one person. In this case, the T cells compete to recognize the different strains, and
recognition of all strains may not be uniformly effective. This immunodominance of one strain over others means
that the immune response to multiple infections is not a simple superposition of the responses to each individual
infection [3].
更多原文鏈接:http://arxiv.org/abs/q-bio.PE/0610018
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