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

Author:

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

Abstract

AbstractThe 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 compoundDrosophilaeye 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 3rdchromosome 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.

Publisher

Cold Spring Harbor Laboratory

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