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SAGA has been found to be a necessary target of Ga14p, the yeast acidic activator, in vivo and to facilitate PIC assembly and transcription after recruitment to the upstream activating sequence (UAS). A study was carried out using formaldehyde-based in vivo cross linking.

Pyruvate metabolism in intact Halobacterium salinarium cells is studied by 13 C NMR spectroscopy. The metabolism involves pyruvate transamination to alanine and reduction to lactic acid. NADH-dependent lactate dehydrogenase function of the cells is reduced in the absence of glucose. Acetyl-coenzyme A induces pyruvate insertion into tricarbonylic acid cycle causing fumarate-succinate stage phase label scrambling, malic enzyme activity and carboxylase-type reaction. H. salinarium growth influences citrate synthase and malic enzyme function.

Although an F-box protein, Mdm30, is found to regulate ubiquitylation of the Sub2 component of TREX (TRanscription-EXport) complex for proteasomal degradation in stimulation of mRNA export, it remains unknown whether such ubiquitin-proteasome system (UPS) regulation of Sub2 occurs co-transcriptionally via its interaction with Mdm30. Further, it is unclear whether impaired UPS regulation of Sub2 in absence of Mdm30 alters mRNA export via splicing defects of export factors and/or mitochondrial dynamics/function, since Sub2 controls mRNA splicing and Mdm30 regulates mitochondrial aggregation. Here, we show that Mdm30 interacts with Sub2, and temporary shut-down of Mdm30 enhances Sub2's abundance and impairs mRNA 40 export. Likewise, Sub2's abundance is increased following transcriptional inhibition. These results support Mdm30's direct role in regulation of Sub2's cellular abundance in transcription-dependent manner. Consistently, chromatin-bound Sub2 level is increased in absence of Mdm30. Further, we find that Mdm30 does not facilitate splicing of export factors. Moreover, Mdm30 does not have dramatic effect on mitochondrial respiration/function, and mRNA export occurs in absence of Fzo1 that is required for mitochondrial dynamics/respiration. Collective results reveal that Mdm30 interacts with Sub2 for proteasomal degradation in transcription-dependent manner to promote mRNA export independently of splicing or mitochondrial function, thus advancing our understanding of mRNA export. [ABSTRACT FROM AUTHOR]

Interaction of Gal4-Tral is found essential for recruitment of SAGA (Spt/Ada/Gen5/acetyltransferase) to the upstream activating sequence (UAS) and SAGA in turn recruits the Mediator complex to the UAS. Studies reflect the process of transcriptional stimulation via activator-target interaction.

Non-coding antisense transcripts arise from the strand opposite the sense strand. Over 70% of the human genome generates non-coding antisense transcripts while less than 2% of the genome codes for proteins. Antisense transcripts and/or the act of antisense transcription regulate gene expression and genome integrity by interfering with sense transcription and modulating histone modifications or DNA methylation. Hence, they have significant pathological and physiological relevance. Indeed, antisense transcripts were found to be associated with various diseases including cancer, diabetes, cardiac and neurodegenerative disorders, and, thus, have promising potentials for prognostic and diagnostic markers and therapeutic development. However, it is not clearly understood how antisense transcription is initiated and epigenetically regulated. Such knowledge would provide new insights into the regulation of antisense transcription, and hence disease pathogenesis with therapeutic development. The recent studies on antisense transcription initiation and its epigenetic regulation, which are limited, are discussed here. Furthermore, we concisely describe how antisense transcription/transcripts regulate gene expression and genome integrity with implications in disease pathogenesis and therapeutic development. [ABSTRACT FROM AUTHOR]