Casta Louis J, Buguliskis Jeffery S, Matsumoto Yoshihiro, Taraschi Theodore F
Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107-6731, USA.
Mol Biochem Parasitol. 2008 Jan;157(1):1-12. doi: 10.1016/j.molbiopara.2007.08.008. Epub 2007 Sep 2.
Flap endonuclease-1 (FEN-1) is a structure-specific endonuclease that is critical for the resolution of single-stranded DNA flap intermediates that form during long patch DNA base excision repair (BER). This investigation reports that Plasmodium species encode FEN-1 homologs. Protein sequence analysis revealed the N and I domains of Plasmodium falciparum (PfFEN-1) and Plasmodium yoelii (PyFEN-1) to be homologous to FEN-1 from other species. However, each possessed an extended C domain which had limited homology to apicomplexan FEN-1s and no homology to eukaryotic FEN-1s. A conserved proliferating cell nuclear antigen (PCNA)-binding site was identified at an internal location rather than the extreme C-terminal location typically seen in FEN-1 from other organisms. The endonuclease and exonuclease activities of PfFEN-1 and PyFEN-1 were investigated using recombinant protein produced in Escherichia coli. Pf and PyFEN-1 possessed DNA structure-specific flap endonuclease and 5'-->3' exonuclease activities, similar to FEN-1s from other species. Endonuclease activity was stimulated by Mg(2+) or Mn(2+) and inhibited by monovalent ions (>20.0 mM). A PfFEN-1 C-terminal truncation mutant lacking the terminal 250 amino acids (PfFEN-1DeltaC) had endonuclease activity that was approximately 130-fold greater (k(cat)=1.2x10(-1)) than full-length PfFEN-1 (k(cat)=9.1x10(-4)) or approximately 240-fold greater than PyFEN-1 (k(cat)=4.9x10(-4)) in vitro. PfFEN-1 generated a nicked DNA substrate that was ligated by recombinant Pf DNA Ligase I (PfLigI) using an in vitro DNA repair assay. Plasmodium FEN-1s have enzymatic activities similar to other species but contain extended C-termini and a more internally located PCNA-binding site.
瓣内切核酸酶-1(FEN-1)是一种结构特异性内切核酸酶,对于在长片段DNA碱基切除修复(BER)过程中形成的单链DNA瓣状中间体的拆分至关重要。本研究报告疟原虫属编码FEN-1同源物。蛋白质序列分析显示,恶性疟原虫(PfFEN-1)和约氏疟原虫(PyFEN-1)的N结构域和I结构域与其他物种的FEN-1同源。然而,它们各自都有一个延长的C结构域,该结构域与顶复门FEN-1的同源性有限,与真核生物FEN-1没有同源性。在内部位置而非其他生物体的FEN-1中通常可见的极端C末端位置鉴定到一个保守的增殖细胞核抗原(PCNA)结合位点。使用在大肠杆菌中产生的重组蛋白研究了PfFEN-1和PyFEN-1的内切核酸酶和外切核酸酶活性。PfFEN-1和PyFEN-1具有DNA结构特异性瓣内切核酸酶和5'→3'外切核酸酶活性,类似于其他物种的FEN-1。内切核酸酶活性受到Mg(2+)或Mn(2+)的刺激,并受到单价离子(>20.0 mM)的抑制。缺少末端250个氨基酸的PfFEN-1 C末端截短突变体(PfFEN-1DeltaC)在体外的内切核酸酶活性比全长PfFEN-1(k(cat)=9.1x10(-4))高约130倍(k(cat)=1.2x10(-1)),比PyFEN-1(k(cat)=4.9x10(-4))高约240倍。PfFEN-1产生了一个带切口的DNA底物,该底物在体外DNA修复试验中被重组Pf DNA连接酶I(PfLigI)连接。疟原虫FEN-1具有与其他物种相似的酶活性,但含有延长的C末端和更位于内部的PCNA结合位点。