Abstract

DNA replication and repair are two fundamental processes required in life proliferation and cellular defense and some common proteins are involved in both processes. The filamentous cyanobacterium Anabaena sp. strain PCC 7120 is capable of forming heterocysts for N2 fixation in the absence of a combined-nitrogen source. This developmental process is intimately linked to cell cycle control. In this study, we investigated the localization of the DNA double-strand break repair protein RecN during key cellular events, such as chromosome damaging, cell division, and heterocyst differentiation. Treatment by a drug causing DNA double-strand breaks (DSBs) induced reorganization of the RecN focus preferentially towards the mid-cell position. RecN-GFP was absent in most mature heterocysts. Furthermore, our results showed that HetR, a central player in heterocyst development, was involved in the proper positioning and distribution of RecN-GFP. These results showed the dynamics of RecN in DSB repair and suggested a differential regulation of DNA DSB repair in vegetative cell and heterocysts. The absence of RecN in mature heterocysts is compatible with the terminal nature of these cells.

Highlights

  • DNA repairing is essential for keeping the integrity of chromosome for cell survival

  • DNA double-strand breaks (DSBs), including one-ended DSBs and two-ended DSBs can be repaired by homologous recombination (HR), whereas two-ended DSBs can be repaired by nonhomologous end-joining or single-strand annealing

  • To examine how DNA repair operates in cyanobacteria with terminal differentiation, we focused on the RecN of Anabaena

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Summary

Introduction

DNA repairing is essential for keeping the integrity of chromosome for cell survival. DNA double-strand breaks (DSBs), including one-ended DSBs and two-ended DSBs can be repaired by homologous recombination (HR), whereas two-ended DSBs can be repaired by nonhomologous end-joining or single-strand annealing. More and more gained details have provided a better understanding of this stepwise process in bacteria [1,2,3,4,5], and the advance of fluorescent tracking technology has allowed the related proteins to be directly visualized in situ [6,7,8]. The understanding of the DNA DSB repairing process is not very clear.

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