We have studied a mutant strain of Drosophila in which 80% of the mitochondrial DNA molecules have lost over 30% of their coding region through deletion. This deletion affects genes encoding five subunits of complex I of the respiratory chain (NADH:ubiquinone oxidoreductase). The enzymatic activity of complex I in the mutant strain is half that in the wild strain, but ATP synthesis is unaffected. The drop in enzymatic activity of complex I in the mutant strain is associated with a 50% decrease in the quantity of constitutive proteins of the complex. Moreover, in the mutant strain there is a 50% decrease in the steady-state concentration of the transcripts of the mitochondrial genes affected by the deletion. This decrease is also observed for the transcripts of the nuclear genes coding for the subunits of complex I. These results suggest a coordination of the expression of the mitochondrial and nuclear genes coding for mitochondrial proteins.
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http://dx.doi.org/10.1023/b:jobb.0000023624.06665.40 | DOI Listing |
Int J Mol Sci
December 2024
CAS Key Laboratory for Quantitative Engineering Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China.
Recently, we developed a spatial phage-assisted continuous evolution (SPACE) system. This system utilizes chemotaxis coupled with the growth of motile bacteria during their spatial range expansion in soft agar to provide fresh host cells for iterative phage infection and selection pressure for preserving evolved genes of interest carried by phage mutants. Controllable mutagenesis activated only in a subpopulation of the migrating cells is essential in this system to efficiently generate mutated progeny phages from which desired individuals are selected during the directed evolution process.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Microbiology and Parasitology, Pharmacy Faculty at Complutense University of Madrid, 28040 Madrid, Spain.
Extracellular vesicles (EVs) from can elicit immune responses, positioning them as promising acellular vaccine candidates. We characterized EVs from an avirulent cell wall mutant (Δ) and evaluated their protective potential against invasive candidiasis. EVs from the yeast (YEVs) and hyphal (HEVs) forms of the SC5314 wild-type strain were also tested, yielding high survival rates with SC5314 YEV (91%) and YEV immunization (64%).
View Article and Find Full Text PDFInt J Mol Sci
December 2024
College of Resources and Environment, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Microbes have been shown to adapt to stressful or even lethal conditions through displaying genome plasticity. However, how bacteria utilize the ability of genomic plasticity to deal with high antimony (Sb) stress has remained unclear. In this study, the spontaneous mutant strain SMAs-55 of sp.
View Article and Find Full Text PDFJ Agric Food Chem
January 2025
Key Laboratory of Industrial Fermentation Microbiology (Ministry of Education), Tianjin University of Science & Technology, Tianjin 300457, People's Republic of China.
Cyclic diguanosine monophosphate (c-di-GMP) is a crucial secondary messenger that regulates bacterial cellulose (BC) synthesis. It is synthesized by diguanylate cyclase (DGC) containing a Gly-Gly-Asp/Glu-Glu-Phe (GGDEF) domain and degraded by phosphodiesterase (PDE) with a Glu-Ala-Leu (EAL) domain. In this work, a systematic analysis of ten GGDEF-EAL tandem domain proteins from CGMCC 2955 assessed their c-di-GMP metabolic functions and effects on BC titer and structure.
View Article and Find Full Text PDFJ Mol Cell Cardiol
January 2025
Shu Chien-Gene Lay Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA; Institute of Engineering Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Sanford Consortium for Regenerative Medicine, La Jolla, CA 92093, USA. Electronic address:
Vinculin (VCL) is a key adapter protein located in force-bearing costamere complexes, which mechanically couples the sarcomere to the ECM. Heterozygous vinculin frameshift genetic variants can contribute to cardiomyopathy when external stress is applied, but the mechanosensitive pathways underpinning VCL haploinsufficiency remain elusive. Here, we show that in response to extracellular matrix stiffening, heterozygous loss of VCL disrupts force-mediated costamere protein recruitment, thereby impairing cardiomyocyte contractility and sarcomere organization.
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