A genome-wide CRISPR screen identifies DPM1 as a modifier of DPAGT1 deficiency and ER stress
Fig 4
Knockdown of glycosylation pathways rescues the DPAGT1 and ER stress models.
(A) A summary of RNAi data performed on downstream DPM1 glycosylation pathways. The majority of mannosyltransferases tested in O-mannosylation, N-glycosylation, and GPI anchor biosynthesis pathways increased eye size in the DPAGT1 model. Colors denote % change of eye size vs their control; warmer colors (or up-arrows) have a stronger effect, and vice versa. Colors are derived from the averages of at least 2 biological replicates with at least one significant replicate and no opposite results (see S7 Table for all RNAi data). * = One PIG-M RNAi line was very strong (BDSC 51890), while a second line was neutral/negative in response (see S7 Table). (B) Representative images of the DPAGT1 model crossed with RNAi against the two strongest hits, tw and PIG-M. Shown are three representative images from the same RNAi line and experimental cross (tw: BDSC 55735, PIG-M: BDSC 51890) or control RNAi background (attP40: BDSC 36304). (C) Quantification of tw and PIG-M rescue shown in B. For reference, the total quantification of that experiment, as well as a representative wild type DPAGT1 genetically-matched background strain crossed to the control RNAi line, is included. ** p<0.01, *** p<0.001 (Student’s t test).