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. 2019 Mar 13;212(1):187–211. doi: 10.1534/genetics.119.302051

Table 5. Candidate genes screened for interaction with sas-4.

RNAi gene target Stock identified Crossed to MS>GFP alone Crossed to MS>GFP;sas-4 RNAi
Upd2 BDSC 33949 Strongly dysmorphic Strongly dysmorphic
BDSC 33988 Not determined Normal
Ets21C BDSC 39069 Strongly dysmorphic Strongly dysmorphic
Castor VDRC 2929 Normal Normal
Cnc VDRC 37674 Normal Normal
VDRC 108127 Normal Normal
VDRC 101235 Strongly dysmorphic Strongly dysmorphic
Dif VDRC 30579 Normal Normal
VDRC 100537 Normal Normal
G6PD VDRC 101507 All erect, 5% blistered and 7% furled All erect, 29% blistered and 11% furled
BDSC 50667 Strongly dysmorphic Strongly dysmorphic
ImpL3 VDRC 110190 Normal Normal
VDRC 31192 Normal Normal
Jra VDRC 31595 Normal Necrotic spots
KEAP1 VDRC 107052 Normal Normal
VDRC 330323 Normal Normal
TRAF4 VDRC 110766 Normal Normal
MMP1 VDRC 31989 Normal Normal
WWOX VDRC 108350 Normal Normal

Based on cellular function, a subset of genes was selected from the list of genes that were upregulated in both sas-4 and asl mutants relative to wild-type. The stock identifiers for RNAi lines targeting the genes of interest are shown. RNAi lines were crossed to the MS1096-Gal4 UAS-GFP (MS>GFP) wing disc driver alone and in combination with sas-4 RNAi. Glucose-6-phosphate dehydrogenase knockdown alone had modest effects that were synergistically elevated in cells codepleted of centrosomes by sas-4 RNAi (see Figure 6, A and B). RNAi, RNA interference; BDSC, Bloomington Drosophila Stock Center; VDRC, Vienna Drosophila Resource Center.