Loenen Wil A M
Department of Medical Microbiology, University Maastricht, Maastricht, The Netherlands.
Nucleic Acids Res. 2003 Dec 15;31(24):7059-69. doi: 10.1093/nar/gkg944.
1953 was a historical year for biology, as it marked the birth of the DNA helix, but also a report by Bertani and Weigle on 'a barrier to infection' of bacteriophage lambda in its natural host, Escherichia coli K-12, that could be lifted by 'host-controlled variation' of the virus. This paper lay dormant till Nobel laureate Arber and PhD student Dussoix showed that the lambda DNA was rejected and degraded upon infection of different bacterial hosts, unless it carried host-specific modification of that DNA, thus laying the foundations for the phenomenon of restriction and modification (R-M). The restriction enzyme of E.coli K-12, EcoKI, was purified in 1968 and required S-adenosylmethionine (AdoMet) and ATP as cofactors. By the end of the decade there was substantial evidence for a chromosomal locus hsdK with three genes encoding restriction (R), modification (M) and specificity (S) subunits that assembled into a large complex of >400 kDa. The 1970s brought the message that EcoKI cut away from its DNA recognition target, to which site the enzyme remained bound while translocating the DNA past itself, with concomitant ATP hydrolysis and subsequent double-strand nicks. This translocation event created clearly visible DNA loops in the electron microscope. EcoKI became the archetypal Type I R-M enzyme with curious DNA translocating properties reminiscent of helicases, recognizing the bipartite asymmetric site AAC(N6)GTGC. Cloning of the hsdK locus in 1976 facilitated molecular understanding of this sophisticated R-M complex and in an elegant 'pas de deux' Murray and Dryden constructed the present model based on a large body of experimental data plus bioinformatics. This review celebrates the golden anniversary of EcoKI and ends with the exciting progress on the vital issue of restriction alleviation after DNA damage, also first reported in 1953, which involves intricate control of R subunit activity by the bacterial proteasome ClpXP, important results that will keep scientists on the EcoKI track for another 50 years to come.
1953年对生物学来说是具有历史意义的一年,这一年标志着DNA双螺旋结构的诞生,同时也有贝塔尼和韦格尔关于噬菌体λ在其天然宿主大肠杆菌K - 12中存在“感染障碍”的报告,而这种障碍可以通过病毒的“宿主控制变异”来消除。这篇论文一直未被关注,直到诺贝尔奖获得者阿伯和博士生杜索伊发现,λDNA在感染不同细菌宿主时会被排斥和降解,除非它携带了该DNA的宿主特异性修饰,从而为限制与修饰(R - M)现象奠定了基础。大肠杆菌K - 12的限制酶EcoKI于1968年被纯化,它需要S - 腺苷甲硫氨酸(AdoMet)和ATP作为辅助因子。到20世纪60年代末,有大量证据表明存在一个染色体位点hsdK,它有三个基因分别编码限制(R)、修饰(M)和特异性(S)亚基,这些亚基组装成一个大于400 kDa的大型复合物。20世纪70年代有消息称,EcoKI在远离其DNA识别靶点的位置切割,在将DNA移位通过自身的过程中,酶仍与该位点结合,同时伴随着ATP水解和随后的双链切口。这种移位事件在电子显微镜下产生了清晰可见的DNA环。EcoKI成为了典型的I型R - M酶,具有类似于解旋酶的奇特DNA移位特性,识别二分不对称位点AAC(N6)GTGC。1976年hsdK位点的克隆促进了对这种复杂R - M复合物的分子理解,默里和德莱登基于大量实验数据和生物信息学构建了目前的模型,宛如一场优雅的“双人舞”。这篇综述纪念EcoKI发现五十周年,并以DNA损伤后限制缓解这一重要问题上令人兴奋的进展作为结尾,这一问题同样首次报道于1953年,它涉及细菌蛋白酶体ClpXP对R亚基活性的复杂调控,这些重要成果将使科学家们在未来50年里继续关注EcoKI。