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Mutation of a novel ABC transporter gene is responsible for the failure to incorporate uric acid in the epidermis of ok mutants of the silkworm, Bombyx mori.

Abstract：

:ok mutants of the silkworm, Bombyx mori, exhibit highly translucent larval skin resulting from the inability to incorporate uric acid into the epidermal cells. Here we report the identification of a gene responsible for the ok mutation using positional cloning and RNAi experiments. In two independent ok mutant strains, we found a 49-bp deletion and a 233-bp duplication, respectively, in mRNAs of a novel gene, Bm-ok, which encodes a half-type ABC transporter, each of which results in translation of a truncated protein in each mutant. Although the Bm-ok sequence was homologous to well-known transporter genes, white, scarlet, and brown in Drosophila, the discovery of novel orthologs in the genomes of lepidopteran, hymenopteran, and hemipteran insects identifies it as a member of a new distinct subfamily of transporters. Embryonic RNAi of Bm-ok demonstrated that repression of Bm-ok causes a translucent phenotype in the first-instar silkworm larva. We discuss the possibility that Bm-ok forms a heterodimer with another half-type ABC transporter, Bmwh3, and acts as a uric acid transporter in the silkworm epidermis.

journal_name

Insect Biochem Mol Biol

journal_title

Insect biochemistry and molecular biology

authors

Wang L,Kiuchi T,Fujii T,Daimon T,Li M,Banno Y,Kikuta S,Kikawada T,Katsuma S,Shimada T

doi

10.1016/j.ibmb.2013.03.011

subject

Has Abstract

pub_date

2013-07-01 00:00:00

pages

562-71

issue

7

eissn

0965-1748

issn

1879-0240

pii

S0965-1748(13)00054-4

journal_volume

43

pub_type

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