為什么進化的速度以及復雜性變得越來越快,?根據(jù)化石記錄顯示,,單細胞生物于35億年前首次出現(xiàn)在地球上,但是之后它們用了大約25億年進化成多細胞生物,,剩下的10億年卻發(fā)展成了植物,、哺乳動物、昆蟲,、鳥類等各種各樣的地球物種。
Rice大學科學家的研究結果可望解決這一問題,,他們認為生物進化速度的加快是因為細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達到如此快速度的,。
Rice大學的Michael Deem說:“我們創(chuàng)造了第一個能解釋物種間基因交換的進化數(shù)學模型,。”結果發(fā)表在了1月29日的《Physical Review Letters》上。過去的數(shù)學模型主要關注生物如何對點突變做出反應,,很少的理論關注再結合過程,。
基因水平轉移(HGT)是物種間的基因轉移,是DNA從一個物種轉移另一個物種,。在50年前這一想法首次被提出時受到科學家的嘲笑,,但是細菌抗藥性的出現(xiàn)以及其它的很多發(fā)現(xiàn),包括細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過程對于進化動力學的影響,。過去的模型只能解釋點變異,,Deem和Park的模型顯示了HGT如何通過傳遞變異增加進化的速度。
在一月的《Physics Today》上,,Deem就描述了HGT的重要性,,例如幫助細菌擁有對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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