RESUMO
The functions of several SOS regulated genes in Escherichia coli are still unknown, including dinQ. In this work we characterize dinQ and two small RNAs, agrA and agrB, with antisense complementarity to dinQ. Northern analysis revealed five dinQ transcripts, but only one transcript (+44) is actively translated. The +44 dinQ transcript translates into a toxic single transmembrane peptide localized in the inner membrane. AgrB regulates dinQ RNA by RNA interference to counteract DinQ toxicity. Thus the dinQ-agr locus shows the classical features of a type I TA system and has many similarities to the tisB-istR locus. DinQ overexpression depolarizes the cell membrane and decreases the intracellular ATP concentration, demonstrating that DinQ can modulate membrane-dependent processes. Augmented DinQ strongly inhibits marker transfer by Hfr conjugation, indicating a role in recombination. Furthermore, DinQ affects transformation of nucleoid morphology in response to UV damage. We hypothesize that DinQ is a transmembrane peptide that modulates membrane-dependent activities such as nucleoid compaction and recombination.
Assuntos
Membrana Celular , Proteínas de Escherichia coli/genética , Escherichia coli , Proteínas de Membrana/genética , RNA Bacteriano , Membrana Celular/genética , Membrana Celular/metabolismo , Membrana Celular/efeitos da radiação , Citoplasma , Dano ao DNA/efeitos da radiação , Escherichia coli/genética , Escherichia coli/metabolismo , Proteínas de Escherichia coli/metabolismo , Regulação Bacteriana da Expressão Gênica/efeitos da radiação , Peptídeos/genética , Peptídeos/metabolismo , RNA Antissenso/genética , RNA Antissenso/metabolismo , RNA Bacteriano/genética , RNA Bacteriano/metabolismo , Recombinação Genética/genética , Resposta SOS em Genética/efeitos da radiação , Transativadores/genética , Transativadores/metabolismo , Raios UltravioletaRESUMO
BACKGROUND: Toll-like receptors (TLRs) are key pattern-recognition receptors of the innate immune system, but their role in human immunodeficiency virus (HIV) infection is largely unknown. METHODS: In the present study, we examined the expression of TLR2 and TLR4 on monocytes from 48 HIV-infected patients and 21 healthy control subjects by flow cytometry. RESULTS: We found that freshly isolated monocytes from HIV-infected patients displayed enhanced expression of TLR2 but not TLR4, that TLR2 expression on the surface of monocytes was significantly increased upon stimulation of HIV type 1 envelope protein gp120, and that TLR2 stimulation in HIV-infected patients induced increased viral replication and TNF- alpha response. CONCLUSION: Our findings suggest potential roles for TLR2 in chronic immune activation and viral replication in HIV infection.