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N-Glycosylation Protects Host from Mycobacterial Infection https://doi.org/10.17863/CAM.112837 Lyu, Bingnan Ramakrishnan, Lalita Host immunity against tuberculosis (TB) is primarily mediated by macrophages. Macrophages phagocytose *Mycobacterium tuberculosis* and restrict their growth. Through a zebrafish forward genetic screen, we have identified the early steps of N-glycosylation are required for the macrophage to resist mycobacterial infections. N-glycosylation attaches an oligosaccharide molecule to nascent secretory or membrane proteins within the endoplasmic reticulum (ER) for protein folding and trafficking. Defects of N-glycosylation induce the unfolded protein response (UPR), which sensitizes infected macrophages to intrinsic apoptosis. This apoptosis differs from the cell death observed in infected wild-type cells and is not dependent on mycobacterial virulence factors. Therefore, N-glycosylation provides protection by mitigating the ER stress of protein synthesis triggered by cellular responses to mycobacterial infection. University of Cambridge 2024-03-29 Thesis Doctoral Doctor of Philosophy (PhD) eng https://www.repository.cam.ac.uk/handle/1810/374983 embargo 2025-10-18 https://apollo8-f-pro.lib.cam.ac.uk/bitstreams/e7eb227e-6466-47d8-b96b-84d8af5741be/download 87a2addb5959e3c8e9bf1b01f3f6dcef https://apollo8-f-pro.lib.cam.ac.uk/bitstreams/896d9b2b-7444-4eb4-affe-1b9416992367/download 87eda9de84448d1f82354d60eee3eb5f https://www.rioxx.net/licenses/all-rights-reserved/ Cell Death ER Stress Macrophage N-glycosylation Tuberculosis