Michelle Bland

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Primary Appointment

Associate Professor, Pharmacology

Education

  • PhD, University of California, San Francisco

Research Disciplines

Genetics, Immunology, Metabolism, Molecular Pharmacology, Translational Science

Research Interests

Molecular mechanisms linking innate immune and insulin signaling to control cell growth and metabolism

Research Description

Infection in the juvenile stage disrupts growth and metabolism, often with long-lasting effects. In young children and in fruit fly larvae, infections disrupt production of homologous hormones: insulin-like growth factor 1 (IGF1) and Drosophila insulin-like peptide 6 (Dilp6), leading to reduced whole-animal growth. Infections also dramatically alter carbohydrate and lipid metabolism. In humans, a life-long effect of early childhood infections is increased risk of metabolic syndrome.
Our lab uses genetic approaches in flies and in mice to identify molecular mechanisms linking infection and innate immune signaling with disrupted growth and metabolism. We are working to identify transcriptional mechanisms that lead to decreased IGF1 and Dilp6 production in response to infection.
Our lab also identified that innate immune signaling induces phospholipid synthesis in a key immune organ, the fruit fly larval fat body, that is required for successfully combatting infection. We are working to identify components of the Toll signaling pathway that link infection with changes in cellular lipid metabolism.
A third major focus of the lab is to identify endocrine mechanisms that allow animals to adapt to distinct environmental challenges, whether due to infection or nutrient stress. Here we are working to determine roles of two highly related homologs, Dilp2, secreted by fourteen insulin-producing cells in the Drosophila larval brain, and Dilp6, secreted by the larval fat body, in regulating growth and metabolism.

Personal Statement

Infection in the juvenile stage disrupts growth and metabolism, often with long-lasting effects. In young children and in fruit fly larvae, infections disrupt production of homologous hormones: insulin-like growth factor 1 (IGF1) and Drosophila insulin-like peptide 6 (Dilp6), leading to reduced whole-animal growth. Infections also dramatically alter carbohydrate and lipid metabolism. In humans, a life-long effect of early childhood infections is increased risk of metabolic syndrome.
Our lab uses genetic approaches in flies and in mice to identify molecular mechanisms linking infection and innate immune signaling with disrupted growth and metabolism. We are working to identify transcriptional mechanisms that lead to decreased IGF1 and Dilp6 production in response to infection.
Our lab also identified that innate immune signaling induces phospholipid synthesis in a key immune organ, the fruit fly larval fat body, that is required for successfully combatting infection. We are working to identify components of the Toll signaling pathway that link infection with changes in cellular lipid metabolism.
A third major focus of the lab is to identify endocrine mechanisms that allow animals to adapt to distinct environmental challenges, whether due to infection or nutrient stress. Here we are working to determine roles of two highly related homologs, Dilp2, secreted by fourteen insulin-producing cells in the Drosophila larval brain, and Dilp6, secreted by the larval fat body, in regulating growth and metabolism.

Training

  • Training in the Pharmacological Sciences

Selected Publications

2022

Bland, M. L. (2022). Regulating metabolism to shape immune function: Lessons from Drosophila.. Seminars in cell & developmental biology, S1084-9521(22)00127-6. doi:10.1016/j.semcdb.2022.04.002

2020

Martinez, B. A., Hoyle, R. G., Yeudall, S., Granade, M. E., Harris, T. E., Castle, J. D., . . . Bland, M. L. (2020). Innate immune signaling in Drosophila shifts anabolic lipid metabolism from triglyceride storage to phospholipid synthesis to support immune function. PLOS GENETICS, 16(11). doi:10.1371/journal.pgen.1009192

Raje, V., Ahern, K. W., Martinez, B. A., Howell, N. L., Oenarto, V., Granade, M. E., . . . Harris, T. E. (2020). Adipocyte lipolysis drives acute stress-induced insulin resistance. SCIENTIFIC REPORTS, 10(1). doi:10.1038/s41598-020-75321-0

Yuan, X., Sipe, C. W., Suzawa, M., Bland, M. L., & Siegrist, S. E. (2020). Dilp-2-mediated PI3-kinase activation coordinates reactivation of quiescent neuroblasts with growth of their glial stem cell niche. PLOS BIOLOGY, 18(5). doi:10.1371/journal.pbio.3000721

2019

Suzawa, M., Muhammad, N. M., Joseph, B. S., & Bland, M. L. (2019). The Toll Signaling Pathway Targets the Insulin-like Peptide Dilp6 to Inhibit Growth in Drosophila. CELL REPORTS, 28(6), 1439-+. doi:10.1016/j.celrep.2019.07.015

2018

Roth, S. W., Bitterman, M. D., Birnbaum, M. J., & Bland, M. L. (2018). Innate Immune Signaling in Drosophila Blocks Insulin Signaling by Uncoupling PI(3,4,5)P-3 Production and Akt Activation. CELL REPORTS, 22(10), 2550-2556. doi:10.1016/j.celrep.2018.02.033

2016

Bland, M. L. (2016). Measurement of Carbon Dioxide Production from Radiolabeled Substrates in Drosophila melanogaster. JOVE-JOURNAL OF VISUALIZED EXPERIMENTS, (112). doi:10.3791/54045