Liu Beiyu, Molina Henrik, Kalume Dario, Pandey Akhilesh, Griffith Jack D, Englund Paul T
Department of Biological Chemistry, Johns Hopkins Medical School, 725 N. Wolfe St., Baltimore, MD 21205, USA.
Mol Cell Biol. 2006 Jul;26(14):5382-93. doi: 10.1128/MCB.00369-06.
Trypanosomes have an unusual mitochondrial genome, called kinetoplast DNA, that is a giant network containing thousands of interlocked minicircles. During kinetoplast DNA synthesis, minicircles are released from the network for replication as theta-structures, and then the free minicircle progeny reattach to the network. We report that a mitochondrial protein, which we term p38, functions in kinetoplast DNA replication. RNA interference (RNAi) of p38 resulted in loss of kinetoplast DNA and accumulation of a novel free minicircle species named fraction S. Fraction S minicircles are so underwound that on isolation they become highly negatively supertwisted and develop a region of Z-DNA. p38 binds to minicircle sequences within the replication origin. We conclude that cells with RNAi-induced loss of p38 cannot initiate minicircle replication, although they can extensively unwind free minicircles.
锥虫具有一种不同寻常的线粒体基因组,称为动质体DNA,它是一个包含数千个相互连锁的微小环的巨大网络。在动质体DNA合成过程中,微小环从网络中释放出来以θ结构形式进行复制,然后游离的微小环子代重新附着到网络上。我们报告称,一种线粒体蛋白(我们将其命名为p38)在动质体DNA复制中发挥作用。对p38进行RNA干扰(RNAi)会导致动质体DNA丢失,并积累一种名为S组分的新型游离微小环物种。S组分微小环的缠绕程度极低,以至于在分离时它们会变得高度负超螺旋,并形成一个Z-DNA区域。p38与复制起点内的微小环序列结合。我们得出结论,尽管RNAi诱导p38缺失的细胞能够广泛解开游离微小环,但它们无法启动微小环复制。