Genetics of skeletal development and disease
Welcome to the Henke Lab at Emory University. We are part of the Department of Orthopaedics and the Department of Human Genetics at the School of Medicine. In our research we aim to gain new insight into the development and regulation of the skeleton. We use the zebrafish model system and combine forward and reverse genetic approaches to analyze gene function during skeletogenesis, with a focus on osteoclast - osteoblast communication. Understanding the basis of skeletal biology will help to better understand disease etiology and aid in the development of new treatment strategies for skeletal diseases.
Recent Publications
Daponte V, Henke K, Drissi H (2024) “Current perspectives on the multiple roles of osteoclasts: Mechanisms of osteoclast–osteoblast communication and potential clinical implications”. eLife, Apr 9:13:e95083
Islam, K. N., Ajao, A., Venkataramani, K., Rivera, J., Pathania, S., Henke, K. & Siegfried, K. R. (2023) “The RNA-binding protein Adad1 is necessary for germ cell maintenance and meiosis in zebrafish”. PLoS Genet 19, e1010589, 1010589 .
Henke K, Farmer DT, Niu X, Kraus JM, Galloway JL, Youngstrom DW. (2023) “Genetically engineered zebrafish as models of skeletal development and regeneration”. Bone Feb; 167:116611
Meyer-Miner A, Van Gennip J, Henke K, Harris MP, Ciruna B. (2022). “Resolving Primary Pathomechanisms Driving Idiopathic-like Spinal Curvature Using a New Katnb1 Scoliosis Model.” iScience 25 (9): 105028.
Khrystoforova I, Shochat-Carvalho C, Harari R, Henke K, Woronowicz K, Harris MP, Karasik D (2022) “Zebrafish mutants reveal unexpected role of Lrp5 in osteoclast regulation.” Frontiers in Endocrinology, 13:985304.
Hawkins B, Henke K, Harris MP (2021). “Latent developmental potential to form limb-like skeletal structures in zebrafish”. Cell 184(4)
Peskin B, Henke K, Cumplido N, Treaster S, Harris MP, Bagnat M, Arratia G (2020). “Notochordal signals establish phylogenetic Identity of the teleost spine”. Current Biology 30(14).
Rose CD, Pompili D, Henke K, Van Gennip JLM, Meyer-Miner A, Rana R, Gobron S, Harris MP, Nitz M, Ciruna B. (2020) “SCO-Spondin Defects and Neuroinflammation Are Conserved Mechanisms Driving Spinal Deformity across Genetic Models of Idiopathic Scoliosis”. Current Biology 30(12).