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In Bacteria, the transcribed messenger RNA (mRNA) can be directly attached to the first translating ribosome by creating a physical interaction between the ribosome and RNA polymerase (RNAP)1. The lead ribosome, in this transcription-translation complex, regulates the progression of transcription and protects the transcribed mRNA from premature transcription termination or mRNA degradation2. In the coupled system of transcription-translation the lead ribosome closely trails the RNAP, with rates of translation matching the transcription to support the efficient gene expression2. The direct interactions between RNAP and the translational machinery allow them to co-localize in bacterial cell and maintain the genome stability2,3. The recent cryo-electron microscopy structures of RNAP-ribosome derived from an in vitro transcription-translation reaction suggest a key role for accessory transcription factors4,5. Here, the E. coli transcription factors NusG and NusA can interact with RNAP and ribosome, supporting a bridged mode of coupling (Fig. 1). Perhaps the transcription factors interact with 30S small ribosomal subunit during the transition from translation initiation to elongation and help direct RNAP toward the mRNA tunnel entry6. However, it is not yet known how transcription-translation is controlled in bacteria. Perhaps, structured mRNAs during cellular stress can play a major role in coupled systems in terms of RNAP pausing and allowing the leading ribosome to rescue the transcription. Cytoplasmic viruses transcribe and translate their mRNAs in the cytoplasm of the infected cells7. These viruses coordinate viral genome replication and viral assembly within the viral factories in the cytoplasm of the host cell. The viral mRNAs transcribed by viral RNAPs within the viral factories closely associate with host translation initiation and elongation factors7. Considering the co-localization of host translation machinery with viral factories, the viruses can tightly coordinate viral genome replication and viral assembly by indirect coupling of the viral transcription and host translation.