Molecular mapping and characterization of the silkworm apodal mutant.

Peng Chen,Jiang-Bo Song,Xiao-Ling Tong,Song-Zhen He,Cheng Lu,Hai Hu,Fang-Yin Dai,Ting-Ting Gai,Ming-Yue Fu

doi:10.1038/srep18956

Abstract

The morphological diversity of insects is important for their survival; in essence, it results from the differential expression of genes during development of the insect body. The silkworm apodal (ap) mutant has degraded thoracic legs making crawling and eating difficult and the female is sterile, which is an ideal subject for studying the molecular mechanisms of morphogenesis. Here, we confirmed that the infertility of ap female moths is a result of the degradation of the bursa copulatrix. Positional cloning of ap locus and expression analyses reveal that the Bombyx mori sister of odd and bowl (Bmsob) gene is a strong candidate for the ap mutant. The expression of Bmsob is down-regulated, while the corresponding Hox genes are up-regulated in the ap mutant compared to the wild type. Analyses with the dual luciferase assay present a declined activity of the Bmsob promoter in the ap mutant. Furthermore, we demonstrate that Bmsob can inhibit Hox gene expression directly and by suppressing the expression of other genes, including the BmDsp gene. The results of this study are an important contribution to our understanding of the diversification of insect body plan.

Highlights

These reasons, the ap mutant could not mate naturally and required artificial mating to produce normal offspring
We demonstrated that the Bombyx mori sister of odd and bowl (Bmsob) gene is a strong candidate for the B. mori ap mutant which generates multiple defects by fine mapping and gene expression analysis
We examined the relationship between the candidate gene Bmsob and the Hox genes, whose expression are essential for the proper organization of the animal body plan during development, indicating that Bmsob gene can inhibit Hox gene expression directly and indirectly through suppressing other genes, such as BmDsp

Summary

Introduction

These reasons, the ap mutant could not mate naturally and required artificial mating to produce normal offspring. The silkworm E complex mutants, located on chromosome 6 corresponding to the Hox genes, display ectopic legs, abnormal wings and genital system[25,26], implying a relationship between the ap mutant and Hox genes. We investigated the physiological cause of ap female infertility, and identified and characterized the strong candidate gene responsible for the ap mutant. We confirmed that the infertility of ap female moths was due to the degradation of the bursa copulatrix, and demonstrated that the abnormal expression of the Bmsob gene encoding C2H2 zinc finger-containing transcriptional factor should be probably responsible for ap mutant. We found that the Hox genes in the ap mutant are abnormally expressed and verified the Hox genes can be regulated by the Bmsob gene

Methods

Results

Conclusion