Mutations in actin cause a range of human diseases due to specific molecular changes that often alter cytoskeletal function. In this study, imaging of fluorescently tagged proteins using total internal fluorescence (TIRF) microscopy is used to visualize and quantify changes in cytoskeletal dynamics. TIRF microscopy and the use of fluorescent tags also allows for quantification of the changes in cytoskeletal dynamics caused by mutations in actin. Using this technique, quantification of cytoskeletal function in live cells valuably complements in vitro studies of protein function. As an example, missense mutations affecting the actin residue R256 have been identified in three human actin isoforms suggesting this amino acid plays an important role in regulatory interactions. The effects of the actin mutation R256H on cytoskeletal movements were studied using the yeast model. The protein, Aip1, which is known to assist cofilin in actin depolymerization, was tagged with green fluorescent protein (GFP) at the N-terminus and tracked in vivo using TIRF microscopy. The rate of Aip1p movement in both wild type and mutant strains was quantified. In cells expressing R256H mutant actin, Aip1p motion is restricted and the rate of movement is nearly half the speed measured in wild type cells (0.88 ± 0.30 μm/sec in R256H cells compared to 1.60 ± 0.42 μm/sec in wild type cells, p < 0.005).
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http://dx.doi.org/10.3791/51551 | DOI Listing |
Development
January 2025
School of Science, Technische Universität Dresden, 01062 Dresden, Germany.
The elongation of tissues and organs is important for proper morphogenesis in animal development. In Drosophila ovaries, the elongation of egg chambers involves aligned Collagen IV fiber-like structures, a gradient of extracellular matrix stiffness and actin-based protrusion-driven collective cell migration, leading to the rotation of the egg chamber. Egg chamber elongation and rotation depend on the atypical cadherin Fat2.
View Article and Find Full Text PDFAdv Exp Med Biol
January 2025
Cancer Research UK Scotland Centre (Edinburgh), Institute of Genetics & Cancer, University of Edinburgh, Edinburgh, UK.
E-cadherin is a transmembrane protein and central component of adherens junctions (AJs). The extracellular domain of E-cadherin forms homotypic interactions with E-cadherin on adjacent cells, facilitating the formation of cell-cell adhesions, known as AJs, between neighbouring cells. The intracellular domain of E-cadherin interacts with α-, β- and p120-catenins, linking the AJs to the actin cytoskeleton.
View Article and Find Full Text PDFmBio
January 2025
Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.
is an obligate intracellular, tick-borne bacterial pathogen that can cause eschar-associated rickettsiosis in humans. invades host cells, escapes from vacuoles into the cytosol, and undergoes two independent modes of actin-based motility mediated by effectors RickA or Sca2. Actin-based motility of enables bacteria to enter protrusions of the host cell plasma membrane that are engulfed by neighboring host cells.
View Article and Find Full Text PDFBlood Adv
January 2025
The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Cytoskeletal remodeling and mitochondrial bioenergetics play important roles in thrombocytopoiesis and platelet function. Recently, α-actinin-1 mutations have been reported in patients with congenital macrothrombocytopenia. However, the role and underlying mechanism of α-actinin-1 in thrombocytopoiesis and platelet function remain elusive.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Immunology, School of Medicine, UConn Health, Farmington, CT 06030.
Monocytes are critical in controlling tissue infections and inflammation. Monocyte dysfunction contributes to the inflammatory pathogenesis of cystic fibrosis (CF) caused by CF transmembrane conductance regulator (CFTR) mutations, making CF a clinically relevant disease model for studying the contribution of monocytes to inflammation. Although CF monocytes exhibited adhesion defects, the precise mechanism is unclear.
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