Ribosome-Dependent ATPase Interacts with Conserved Membrane Protein in Escherichia coli to Modulate Protein Synthesis and Oxidative Phosphorylation

Elongation factor RbbA is required for ATP-dependent deacyl-tRNA release presumably after each peptide bond formation; however, there is no information about the cellular role. Proteomic analysis in Escherichia coli revealed that RbbA reciprocally co-purified with a conserved inner membrane protein of unknown function, YhjD. Both proteins are also physically associated with the 30S ribosome and with members of the lipopolysaccharide transport machinery. Genome-wide genetic screens of rbbA and yhjD deletion mutants revealed aggravating genetic interactions with mutants deficient in the electron transport chain. Cells lacking both rbbA and yhjD exhibited reduced cell division, respiration and global protein synthesis as well as increased sensitivity to antibiotics targeting the ETC and the accuracy of protein synthesis. Our results suggest that RbbA appears to function together with YhjD as part of a regulatory network that impacts bacterial oxidative phosphorylation and translation efficiency

Activation of Galphai3 and interacting protein, TNFAIP8, inhibits TNFalpha-induced death and promotes transformation in mouse fibroblast

Stimulation of dopamine D2S receptor introduced in Balb/c-3T3 cells induces Galphai3-dependent transformation. Galphai3 interacts with DED2-containing protein, TNFAIP8, in yeast mating and in FLAG-TNFAIP8 transfected Balb/c-3T3 cells. TNFAIP8 inhibits caspase-8 activity and is elevated in certain cancers as well as in metastatic, radiation resistant, chemo-resistant and angiogenic tumours. This study looks at Galphai3 activation of TNFAIP8 leading to the inhibition of TNFalpha-induced cell death in Balb/c-3T3 cells coexpressing D2S and either TNFAIP8 over-expression or TNFAIP8 antisense-knockdown with assays for foci formation, cell death and executioner caspase activation. The data showed D2S increases basal foci formation; this is blocked in TNFAIP8 antisense cells. D2S activation further increases foci formation; also completely blocked in TNFAIP8 antisense cells. D2S activation reduces cell death except in TNFAIP8 antisense cells. D2S activation reduces caspase-active cells. These results show that D2S mediated inhibition of caspase activity and death resulting in transformation is dependent on TNFAIP8

Cybercrime: Concerns, challenges and opportunities

It is widely accepted that technology is an agent of change in the society. If used properly, it can increase productivity and improve our quality of life. However, the current rate of change in technology leaves room for it to be exploited and be used for things it was not meant to do. This includes criminal activities which are carried using technology on the cyberspace that can be classified as cybercrime. Cybercrime or computer crime can be defined as a criminal activity in which computers or computer networks are a tool, a target or a place of criminal activity. Cybercrime can also be defined as the leveraging of information systems and technology to commit larceny, extortion, identity theft, fraud and, in some cases, corporate espionage. In this chapter, we explore the challenges of combating cybercrime given its dynamic, pervasive and international nature. We examine in detail the technical, social and legal factors that are continually shaping the landscape of cybercrime. Further, the chapter consolidates research and practical work in the area of cybercrime, emerging perspectives, paradigms and trends. A deliberate effort is made in making sure that the role of underground economy is clearly spelled out and its contribution to cybercrime is analysed. The impact of new laws which are being quickly enacted without much thought, discussion on the regulatory framework for combating cybercrime and ethical dimension of cybercrime given its global nature are examined. This chapter is expected to stimulate constructive discussions on novel ways of mitigating and promoting research in cybercrime

Large-scale investigation of oxygen response mutants in Saccharomyces cerevisiae

A genome-wide screen of a yeast non-essential gene-deletion library was used to identify sick phenotypes due to oxygen deprivation. The screen provided a manageable list of 384 potentially novel as well as known oxygen responding (anoxia-survival) genes. The gene-deletion mutants were further assayed for sensitivity to ferrozine and cobalt to obtain a subset of 34 oxygen-responsive candidate genes including the known hypoxic gene activator, MGA2. With each mutant in this subset a plasmid based β-galactosidase assay was performed using the anoxic-inducible promoter from OLE1 gene, and 17 gene deletions were identified that inhibit induc