Deletions extending various distances into the ara PC-PBAD regulatory region were studied to define the sites required in vivo for the activity of these promoters. Deletions from the PC side entering the CRP site, which is located from -80 to -120 with respect to the PBAD transcription start site, reduced activity of this promoter. Similarly, deletions entering this site from the PBAD side reduced activity of the PC promoter. Cyclic AMP receptor protein bound at this site apparently functions to stimulate transcription of both flanking promoters.
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http://dx.doi.org/10.1016/0022-2836(84)90437-6 | DOI Listing |
Sci Adv
January 2025
Department of Hematology, Zhongda Hospital, Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing 210096, China.
SPT5 exhibits versatile functions in RNA Pol II promoter proximal pausing, pause release, and elongation in metazoans. However, the mechanism underlying the functional switch of SPT5 during early elongation has not been fully understood. Here, we report that the phosphorylation site-rich domain (PRD)/CTR1 and the prion-like domain (PLD)/CTR2, which are situated adjacent to each other within the C-terminal repeat (CTR) in SPT5, play pivotal roles in Pol II pausing and elongation, respectively.
View Article and Find Full Text PDFSci China Life Sci
January 2025
Department of Endocrinology and Metabolism, Zhujiang Hospital, Southern Medical University, Guangzhou, 510280, China.
Skeletal muscle plays a significant role in both local and systemic energy metabolism. The current investigation aims to explore the role of the Bambi gene in skeletal muscle, focusing on its implications for muscle hypertrophy and systemic metabolism. We hypothesize that skeletal muscle-specific deletion of Bambi induces muscle hypertrophy, improves metabolic performance, and activates thermogenic adipocytes via the reprogramming of progenitor of iWAT, offering potential therapeutic strategies for metabolic syndromes.
View Article and Find Full Text PDFiScience
January 2025
The Wallenberg Laboratory, Institute of Medicine University of Gothenburg Sweden, Gothenburg, Sweden.
Mice with genetic ablation of PI3Kγ are protected from diet-induced obesity. However, the cell type responsible for PI3Kγ action in obesity remains unknown. We generated mice with conditional deletion of PI3Kγ in neurons using the nestin promoter to drive the expression of the Cre recombinase (PI3Kγ mice) and investigated their metabolic phenotype in a model of diet-induced obesity.
View Article and Find Full Text PDFNPJ Syst Biol Appl
January 2025
The Joint BioEnergy Institute, Lawrence Berkeley National Laboratory, Emeryville, CA, 94608, USA.
Genome-scale metabolic models (GSMM) are commonly used to identify gene deletion sets that result in growth coupling and pairing product formation with substrate utilization and can improve strain performance beyond levels typically accessible using traditional strain engineering approaches. However, sustainable feedstocks pose a challenge due to incomplete high-resolution metabolic data for non-canonical carbon sources required to curate GSMM and identify implementable designs. Here we address a four-gene deletion design in the Pseudomonas putida KT2440 strain for the lignin-derived non-sugar carbon source, p-coumarate (p-CA), that proved challenging to implement.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Department of Biochemistry and Molecular Biology, Dalhousie University, Dalhousie Medicine New Brunswick, 355 Campus Ring Road, Saint John, New Brunswick, E2L 4L5, Canada.
Lipid phosphate phosphatase 3 (LPP3) is a membrane-bound enzyme that hydrolyzes lipid phosphates including the bioactive lipid, lysophosphatidic acid (LPA). Elevated circulating LPA production and cellular LPA signaling are implicated in obesity-induced metabolic and cardiac dysfunction. Deletion of LPP3 in the cardiomyocyte increases circulating LPA levels and causes heart failure and mitochondrial dysfunction in mice.
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