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‣ FBXO25-associated nuclear domains: A novel subnuclear structure
‣ Host genetic background affects regulatory T-cell activity that influences the magnitude of cellular immune response against Mycobacterium tuberculosis
‣ Desenvolvimento e avaliação de uma interface adaptativa para ensino de Ciências e Biologia celular; Development and evaluation of an adaptive interface for Science teaching and Cell biology
‣ Analyzing Defects in the Caenorhabditis elegans Nervous System Using Organismal and Cell Biological Approaches
‣ Teaching Cell Biology in the Large-Enrollment Classroom: Methods to Promote Analytical Thinking and Assessment of Their Effectiveness
‣ A Molecular Genetics Laboratory Course Applying Bioinformatics and Cell Biology in the Context of Original Research
‣ Revelation of p53-independent Function of MTA1 in DNA Damage Response via Modulation of the p21WAF1-Proliferating Cell Nuclear Antigen Pathway*
‣ Serine Residues in the Cytosolic Tail of the T-cell Antigen Receptor α-Chain Mediate Ubiquitination and Endoplasmic Reticulum-associated Degradation of the Unassembled Protein*
‣ Somatic Cell Plasticity and Niemann-Pick Type C2 Protein: ADIPOCYTE DIFFERENTIATION AND FUNCTION*
‣ Production of Anti-carbohydrate Antibodies by Phage Display Technologies: POTENTIAL IMPAIRMENT OF CELL GROWTH AS A RESULT OF ENDOGENOUS EXPRESSION*
‣ sFRP2 Suppression of Bone Morphogenic Protein (BMP) and Wnt Signaling Mediates Mesenchymal Stem Cell (MSC) Self-renewal Promoting Engraftment and Myocardial Repair*
‣ Sp1-dependent Activation of HDAC7 Is Required for Platelet-derived Growth Factor-BB-induced Smooth Muscle Cell Differentiation from Stem Cells*
‣ Integrin α1β1 Promotes Caveolin-1 Dephosphorylation by Activating T Cell Protein-tyrosine Phosphatase*
‣ Vascular Smooth Muscle Notch Signals Regulate Endothelial Cell Sensitivity to Angiogenic Stimulation*
‣ Endothelial Krüppel-like Factor 4 Regulates Angiogenesis and the Notch Signaling Pathway*
‣ Characterization of the Stability and Bio-functionality of Tethered Proteins on Bioengineered Scaffolds: IMPLICATIONS FOR STEM CELL BIOLOGY AND TISSUE REPAIR*
‣ Tracking the Subcellular Fate of 20(S)-Hydroxycholesterol with Click Chemistry Reveals a Transport Pathway to the Golgi*
‣ Fungal and oomycete plant pathogens: cell biology
‣ Cell biology: Networks, regulation, pathways
‣ Mechanisms of Chlamydia manipulation of host cell biology revealed through genetic approaches
Chlamydia trachomatis is the most common sexually transmitted bacterial pathogen and is the leading cause of preventable blindness worldwide. Chlamydia is particularly intriguing from the perspective of cell biology because it is an obligate intracellular pathogen that manipulates host cellular pathways to ensure its proliferation and survival. This is achieved through a significant remodeling of the host cell’s internal architecture from within a membrane-bound vacuole, termed the inclusion. However, given a previous lack of tools to perform genetic analysis, the mechanisms by which Chlamydia induces host cellular changes remained unclear. Here I present genetic and molecular mechanisms of chlamydial manipulation of the host cytoskeleton and organelles. Using a forward genetics screen, InaC was identified as a necessary factor for the assembly of an F-actin structure surrounding the inclusion. InaC associated with the vacuolar membrane where it recruited Golgi-specific ARF-family GTPases. Actin dynamics and ARF GTPases regulate Golgi morphology and positioning within cells, and InaC acted to redistribute the Golgi to surround the Chlamydia inclusion. These findings suggest that Chlamydia places InaC at the inclusion-cytosolic interface to recruit host ARF GTPases and F-actin to form a platform for rearranging intracellular organelles around the inclusion. The inclusion is also surrounded by the intermediate filament vimentin and the chlamydial protease CPAF cleaves vimentin in vitro. CPAF-dependent remodeling of vimentin occurred selectively in late stages of the infection. In living cells...