INTRODUCTION

Restriction-Modification (R-M) systems protect the host bacterium by restriction of invading foreign DNA (bacteriophages, conjugative plasmids). The cellular DNA is protected from restriction by modification methylation at the specific sequences recognised by the restriction enzymes. Type I (R-M) enzymes are multimeric and multifunctional molecules consisting of three subunits encoded by the genes hsdR, hsdM and hsdS. All three genes are required for restriction, while only hsdM and hsdS are sufficient for modification. The hsdS gene product (the HsdS subunit) is responsible for recognition of a specific DNA sequence in both restriction and modification reactions. The DNA target sequences of Type I R-M systems have two specific components separated by a non-specific spacer, e.g.: GAA(N₆)PuTCG for EcoRl24I. The Type I R-M systems are divided into three families based on gene order, amino acid conservation and enzymatic properties. Within each family, the hsdR and hsdM genes are largely homologous and thus exchangeable. The hsdS genes share conserved regions which are believed to be responsible for protein-protein interactions with the HsdM and HsdR subunits[1]. Moreover, the anti-restriction protein Ard encoded by some self-transmissible plasmids has amino acid sequence which shares considerable similarity with conserved regions of the HsdS subunit suggesting that this anti-restriction determinant inhibits HsdS-HsdM assembly and, therefore, assembly of the endonuclease (Figure 1) [2].

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© University of Portsmouth
Author Dr Keith Firman,
Page last updated September 28, 2008