Figure 2.

Fly Transportin is essential for proper animal development and dTnpo loss in eyes and wings causes dysmorphisms

(A) Protein sequence comparison of human TNPO2 (hTNPO2) and Drosophila Tnpo (dTnpo) shown as a diagram and a detailed amino acid alignment. All variants are at conserved amino acids (red) except p.Lys118Asn (orange). Symbols in the protein alignment: identical (|), similar (:), different (.), absent (_).

(B) dTnpo mutants (red) created for loss-of-function (LoF) studies include dTnpo^Δ11 (an imprecise excision of the P-element, NP4408), dTnpo^Gly736Asp (an EMS-induced mutation), and a CRIMIC allele. Two independent RNAi lines, RNAi-1 and RNAi-2, were also obtained.

(C) Animals homozygous for dTnpo mutant alleles demonstrate larval lethality due to dTnpo loss. None of the alleles or a large deficiency allele which lacks dTnpo, Df(3L)Exel8101, complement each other. Lethality caused by dTnpo^Δ11 and dTnpo^Gly736Asp can be rescued using a genomic rescue construct, GR^dTnpo.

(D) The FRT/FLP system was used to make mosaic tissue in the fly eye during development. dTnpo^Gly736Asp causes a rough eye phenotype. No homozygous dTnpo^Δ11 mutant tissue is observed, indicating cell lethality. Scale bar = 100 μm.

(E) The FRT/FLP system was used to make mosaic tissue in the developing wing. dTnpo^Gly736Asp causes notch and blister phenotypes. Scale bar = 200 μm.

In (D) and (E), “Control” is yw;; FRT80B. Full fly genotypes for this and following figures are in Data S2. dTnpo-targeting RNAi produce consistent phenotypes (see Figure S1).