Czank, Andreas, and Eric Kubli. 2001. forever young: a gene facilitating the study of the third larval instar of D. melanogaster.. Dros. Inf. Serv. 84: 175.
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forever young: a gene facilitating the study of the third larval instar of D. melanogaster.

Czank, Andreas,1 and Eric Kubli2.  1Swissmedic, Erlachstr. 8, 3000 Berne 9, Switzerland,;  2Corresponding author, Institute for Zoology, University of Zurich, Winterthurerstr. 190, 8057  Zurich, Switzerland;

In our study of the gene sarah (genetic symbol sra; synonym nebula, genetic symbol nla; publication in preparation), we discovered two alleles of the gene forever young (genetic symbol fey). When balanced over TM6B, Tb e, homozygous fey larvae are identifiable by their Tb+ phenotype. Tubby (Tb) causes short, thick individuals; the phenotype is visible in larvae, pupae and adults. fey1 homozygotes, fey2/Df(3R)sbd (see below), and fey1/fey2 trans-heterozygotes develop to the third instar larvae.  Some eventually pupate. Homozygous fey2 animals die at an earlier stage.

The fey phenotype allows studies on behavior and tumorigenesis of third instar larvae.  When placed on food containing 20-hydroxyecdysone (1 µg/ml), most fey homozygotes pupate though morphogenesis is arrested early.  Mixed in the substrate, any chemical can be studied for its potential of inducing pupation.

The two fey alleles were obtained from a P-element reversion experiment where the P-elements in the sra alleles sraP1 and sraP2 were removed.  Originally, fey1 and fey2 had been referred to as sral1 and sral2, respectively, (Czank 1998) as the result of the fact that P-element removal was a "sra allele" that was homozygous lethal and had a sra phenotype in trans-heterozygous sra/sral1 or sra/sral2 animals.  A genomic rescue with a construct containing the sra genomic DNA including the 5’ regulatory sequences was performed.  This rescue construct reverted the sra phenotype (studied in trans-heterozygotes) but not the lethality.  Therefore, we believe that the original P-element removal was imprecise and thus causing a mutant sra allele, and, as an additional effect, caused a mutation in fey.  This is possible as the P-elements in sraP1 and sraP2 have inserted in the large sra intron that might harbor regulatory sequences for fey.  However, we cannot exclude that our rescue construct was lacking stage specific regulatory sequences for sra.  If so, fey would be a lethal sra allele.

The two genes, fey and sra, lie in the same genomic region 89B12.  When fey1 or fey2 is crossed to flies with Df(3R)sbd26, Df(3R)sbd45 or Df(3R)sbd104, no adult fey/Df(3R)sbd trans-heterozygotes are found.  These sbd deletions also uncover sra.  Two stocks are available, UM3 and UM4, the flies have the genotype cn; ry fey1 sra3/TM6B, Tb e and w; fey2 sra4/TM6B, Tb e, respectively.

            References:  Czank, A., 1998,  sarah, a novel gene affecting reproduction of Drosophila melonogaster females:  Phenotype analysis and cloning.  Ph.D. thesis, University of Zurich, Switzerland.