Articles by Anna Franz in JoVE
Long-term In Vivo Tracking of Inflammatory Cell Dynamics Within Drosophila Pupae Helen Weavers1,2, Anna Franz1, Will Wood3, Paul Martin1,4 1School of Biochemistry, Biomedical Sciences, University of Bristol, 2School of Cellular and Molecular Medicine, Biomedical Sciences, University of Bristol, 3MRC Centre for Inflammation Research, University of Edinburgh, Queens Medical Research Institute, 4School of Physiology, Pharmacology, and Neuroscience, Biomedical Sciences, University of Bristol Here we present a protocol for live-imaging wound repair and the associated inflammatory response at high spatio-temporal resolution in vivo. This method utilizes the pupal stage of Drosophila development to enable long-term imaging and tracking of specific cell populations over time and is compatible with efficient RNAi-mediated gene inactivation.
Other articles by Anna Franz on PubMed
Actin is an Evolutionarily-conserved Damage-associated Molecular Pattern That Signals Tissue Injury in ELife. | Pubmed ID: 27871362 Damage-associated molecular patterns (DAMPs) are molecules released by dead cells that trigger sterile inflammation and, in vertebrates, adaptive immunity. Actin is a DAMP detected in mammals by the receptor, DNGR-1, expressed by dendritic cells (DCs). DNGR-1 is phosphorylated by Src-family kinases and recruits the tyrosine kinase Syk to promote DC cross-presentation of dead cell-associated antigens. Here we report that actin is also a DAMP in invertebrates that lack DCs and adaptive immunity. Administration of actin to triggers a response characterised by selective induction of STAT target genes in the fat body through the cytokine Upd3 and its JAK/STAT-coupled receptor, Domeless. Notably, this response requires signalling via Shark, the orthologue of Syk, and Src42A, a Src-family kinase, and is dependent on Nox activity. Thus, extracellular actin detection via a Src-family kinase-dependent cascade is an ancient means of detecting cell injury that precedes the evolution of adaptive immunity.
Fat Body Cells Are Motile and Actively Migrate to Wounds to Drive Repair and Prevent Infection Developmental Cell. | Pubmed ID: 29486196 Adipocytes have many functions in various tissues beyond energy storage, including regulating metabolism, growth, and immunity. However, little is known about their role in wound healing. Here we use live imaging of fat body cells, the equivalent of vertebrate adipocytes in Drosophila, to investigate their potential behaviors and functions following skin wounding. We find that pupal fat body cells are not immotile, as previously presumed, but actively migrate to wounds using an unusual adhesion-independent, actomyosin-driven, peristaltic mode of motility. Once at the wound, fat body cells collaborate with hemocytes, Drosophila macrophages, to clear the wound of cell debris; they also tightly seal the epithelial wound gap and locally release antimicrobial peptides to fight wound infection. Thus, fat body cells are motile cells, enabling them to migrate to wounds to undertake several local functions needed to drive wound repair and prevent infections.