## 1 Introduction  
Antibiotic resistance of bacteria has become one of the major medical problems in recent years [1]. The appearance of many bacterial strains resistant to one or many antibiotics makes this crucial therapy used to combat various infectious diseases less and less effective, resulting in alarming predictions on the possible lack of cures in such cases in the near future [2]. The spreading of antibiotic resistance is caused mainly by the overuse of these therapeutics and the selection of resistant strains. In fact, antibiotic-resistant bacteria occur naturally in the environment, predominantly because they bear genes coding for proteinsable to inactivate antimicrobial compounds, to prevent the penetration of antibiotics to cells or to remove them from cells, or because of mutations that change the antibiotic targets [3]. Plasmids are extrachromosomal genetic elements that are carriers of many antibiotic resistance genes, thus being responsible for both the efficient survival of bacteria in the presence of antibiotics and many events of horizontal gene transfer, causing effective spreading of antibiotic resistance [4]. Among all kinds of plasmids occurring in Gram-negative bacteria, ColE1-like (or ColE1-type) replicons frequently occur under natural conditions, and they can contribute significantly to the transmission of resistance among pathogenic strains. There are many examples of such plasmids isolated from various habitats, either natural or artificially changed by humans [5; 6; 7; 8; 9; 10; 11; 12]. All functions of plasmids depend on their efficient replication in bacterial cells. Therefore, understanding mechanisms of plasmid replication regulation might provide a way to develop new drugs interfering with the propagation of these genetic elements, thus impairing the antibiotic resistance of bacteria and preventing the spread of this feature. Regulation of the replication of CoE1-like plasmids occurring in _Enterobacteriaceae_ (including _Escherichia coli_) involves the DNA replication-origin region and two regulatory RNAs called RNA I and RNA II [13; 14] (Figure 1). The pre-primer RNA II hybridizes with single-stranded (ss)DNA at the origin region due to partial melting of the DNA helix. This step is necessary for the initiation of complementary DNA strand synthesis by DNA polymerase I. However, RNA I competes with ssDNA for RNA II binding, thus acting as a negative regulator of DNA replication initiation (Figure 1). Furthermore, some proteins can modulate RNA I-RNA II interactions. One of them is a plasmid-encoded Rom protein which facilitates the formation of the RNA I-RNA II hybrid [13; 14]. Our previous in vivo studies showed that the Hfq protein, known as an RNA chaperone [15], which is also able to interact with DNA [16], has implications for the regulation of ColE1-like plasmid DNA replication [17]. Namely, the efficiency of replication of ColE1 plasmids has been investigated in wild-type and isogenic _h/q_ mutant strains of _E. coli_, and a significant decrease in the efficiency of transformation of the _A/hfq_ host relative to the wild-type strain was observed. Interestingly, the kinetics of plasmid DNA synthesis in the absence of Hfq depended on the bacterial growth phase [17]. Recent investigations demonstrated that perturbations with ColE1-like plasmid functions in _E. coli_ _h/q_ mutants resulted in significantly altered levels of bacterial resistance to different antibiotics that were not related to effects of Hfq on transcripts derived from antibiotic-resistance genes [18]. These results indicated that the effects of Hfq on ColE1-like plasmid biology might be important for medically-significant features of bacteria, like antibiotic resistance. The biochemical features of _E. coli_ Hfq are unusual, as this small (102 amino acid (aa) residues) protein is especially resistant to high temperatures and exhibits many activities.