A deficiency screen of the 3rd chromosome for dominant modifiers of the Drosophila ER integral membrane protein, Jagunal

Gerson Ascencio, Matthew A. de Cruz, Judy Abuel, Sydney Alvardo, Yuma Arriaga, Emily Conrad, Alonso Castro, Katharine Eichelberger, Laura Galvan, Grace Gundy, Jorge Alberto Inojoza Garcia, Alyssa Jimenez, Nhein Tuyet Lu, Catharine Lugar, Ronnie Marania, Tserendavaa Mendsaikhan,Jose Ortega, Natasha Nand, Nicole S. Rodrigues, Khayla Shabazz, Cynnie Tam, Emannuel Valenciano, Clive Hayzelden,Anthony S. Eritano,Blake Riggs

biorxiv(2022)

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摘要
The mechanism surrounding chromosome inheritance during cell division has been well documented, however, organelle inheritance during mitosis is less understood. Recently, the Endoplasmic Reticulum (ER) has been shown to reorganize during mitosis, dividing asymmetrically in proneuronal cells prior to cell fate selection, indicating a programmed mechanism of inheritance. ER asymmetric partitioning in proneural cells relies on the highly conserved ER integral membrane protein, Jagunal (Jagn). Knockdown of Jagn in the compound Drosophila eye displays a pleotropic rough eye phenotype in 48% of the progeny. To identify genes involved in Jagn dependent ER partitioning pathway, we performed a dominant modifier screen of the 3rd chromosome for enhancers and suppressors of this Jagn RNAi-induced rough eye phenotype. We screened through 181 deficiency lines covering the 3L and 3R chromosomes and identified 12 suppressors and 10 enhancers of the Jagn RNAi phenotype. Based on the functions of the genes covered by the deficiencies, we identified genes that displayed a suppression or enhancement of the Jagn RNAi phenotype. These include Division Abnormally Delayed (Dally), an heparan sulfate proteoglycan, the γ-secretase subunit Presenilin, and the ER resident protein Sec63. Based on our understanding of the function of these targets, there is a connection between Jagn and the Notch signaling pathway. Further studies will elucidate the role of Jagn and identified interactors within the mechanisms of ER partitioning during mitosis.
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