Tipos de daños en el АDN

la empatia es un tema muy confuso entre la sociedad ya que la mayoria de las personas lo confunden con simpatia.

Background

ATPase/Helicases and nucleases play important roles in homologous recombination repair (HRR). Many of the mechanistic details relating to these enzymes and their function in this fundamental and complicated DNA repair process remain poorly understood in archaea. Here we employed Sulfolobus islandicus, a hyperthermophilic archaeon, as a model to investigate the in vivo functions of the ATPase/helicase HerA, the nuclease NurA, and their associated proteins Mre11 and Rad50.

Results

We revealed that each of the four genes in the same operon, mre11, rad50, herA, and nurA, are essential for cell viability by a mutant propagation assay. A genetic complementation assay with mutant proteins was combined with biochemical characterization demonstrating that the ATPase activity of HerA, the interaction between HerA and NurA, and the efficient 5′-3′ DNA end resection activity of the HerA-NurA complex are essential for cell viability. NurA and two other putative HRR proteins: a PIN (PilT N-terminal)-domain containing ATPase and the Holliday junction resolvase Hjc, were co-purified with a chromosomally encoded N-His-HerA in vivo. The interactions of HerA with the ATPase and Hjc were further confirmed by in vitro pull down.

Conclusion

Efficient 5′-3′ DNA end resection activity of the HerA-NurA complex contributes to necessity of HerA and NurA in Sulfolobus, which is crucial to yield a 3′-overhang in HRR. HerA may have additional binding partners in cells besides NurA.

Keywords: Homologous recombination repair; ATPase; Helicase; Nuclease; HerA; NurA; Archaea

Background

Of the various types of DNA lesions, double-strand breaks (DSBs) are one of the most detrimental, capable of causing chromosomal rearrangements and eventually cell death if not repaired appropriately [1]. In eukaryotes, two major DSB repair pathways are known: non-homologous end joining (NHEJ) and homologous recombination (HR). The former is an error-prone process, while the latter mechanism exhibits high fidelity [2]. It has been suggested that in eukaryotes, DSBs that occur in the G1 phase of the cell cycle are most likely to be repaired via NHEJ, while those occurring in the S/G2 phase are preferentially processed via HRR [2],[3].

HRR has been investigated extensively in bacteria and eukaryotes. Bacteria encode multiple pathways for DSB repair, including RecBCD, the primary HRR pathway, SbcC-SbcD, and one backup system, RecFOR [4],[5]. The HRR pathway can be divided into five general steps: (1) recognition of the break sites and formation of a repair center (RC),

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