Katja Brueckner received her PhD. in biology and cell signalling from the European Molecular Biology Laboratory (EMBL) and the University of Heidelberg, Germany. She performed her postdoctoral studies at the EMBL and Harvard Medical School. Katja was a Howard Hughes Medical Institute Associate, long-term post-doctoral fellow of the European Molecular Biology Organization (EMBO) and Human Frontier Science Program (HFSP), and Special Fellow of the Leukemia & Lymphoma Society (LLS). For her post-doctoral studies, the LLS awarded Katja with the Brian P. ODell Memorial Research Award. Since joining the faculty of UCSF in late 2006, Katja has received a Hellman Family Scholar Award, an American Cancer Society Research Scholar Award, an American Heart Association career development award, and she is funded by research grants from the National Science Foundation and the National Institutes of Health.

The Brückner lab addresses fundamental questions in development, homeostasis, and malignant disease, studying paradigms in the invertebrate genetic model organism Drosophila melanogaster. Current research focuses on cell signaling, the role of the microenvironment, hematopoiesis, innate immunity, epithelial-mesenchymal transition, and organ development.

(1) Regulation of hematopoiesis by sensory neurons and their environmental inputs
One of the outstanding questions in animal development, tissue homeostasis and malignant disease is how extrinsic sensory stimuli regulate biological systems through stem cell niches and tissue microenvironments. We address this question using a simple model of hematopoietic sites (hematopoietic pockets) in the Drosophila larva (Makhijani et al. Development 2011; Makhijani et al. Fly 2012; Gold and Brückner, Seminars in Immunology 2015; Makhijani et al. Nature Communications 2017). In this system, blood cells (hemocytes) rely on sensory neuron microenvironments for their localization and trophic survival (Makhijani et al. Development 2011), and hemocyte proliferation is promoted by Activin-b produced by active sensory neurons (Makhijani et al. Nature Communications 2017). Current research focuses on mechanisms of blood cell transdifferentiation, dissecting the role of specific sensory neurons and their environmental activation in this process (Corcoran et al. bioRxiv 2020). We further examine the contribution of other neuron-produced factors on blood cell development and pathologies.

(2) Multi-tissue signaling relays in innate immunity
Innate immunity relies on humoral responses (e.g. expression of antimicrobial peptides (AMPs)) to protect the organism from infection and other pathological conditions. While core signaling pathways of the NFkB family and Jak/Stat signaling are well established in this context, it is far less understood how multiple organs and tissues communicate with each other to elicit powerful local humoral immune responses. We study this question of inter-organ/-tissue communication in immunity using a simple Drosophila model. In adult Drosophila, the biggest reservoir of hemocytes surrounds the extensive respiratory epithelia (tracheal air sacs) of the thorax and head (Sanchez Bosch et al. Dev Cell 2019). The principal role of the adult blood cell system is to relay the trigger of bacterial infection to a humoral immune response in the respiratory epithelia and fat body (Sanchez Bosch et al. Dev Cell 2019). We dissect mechanisms of this relay including the coordination of multiple signaling pathways and signaling in multiple tissues.

(3) Signaling mechanisms of epithelial-mesenchymal transition
Epithelial-mesenchymal transition (EMT) is a transdifferentiation process of epithelial cells undergoing shape- and migratory changes. A poorly understood group of EMT inducers are Bone Morphogenetic Proteins (BMPs), secreted ligands of the TGF-β family. BMP-induced EMT drives organ development and tumor metastasis, e.g. in pancreatic cancer. However, the cell biological effects and cooperating signaling pathways of BMP-induced EMT are still under scrutiny. We investigate this question using a dual Drosophila model consisting of complementary cell-based and in vivo systems. Through RNAi screening, RNAseq and ChIPseq analyses in this cell-based model, we identified new signaling mediators and pathways that cooperate with BMP signaling to induce EMT; findings are confirmed by Drosophila genetics in vivo.