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ten‐a overexpression causes abnormal pattern in the Drosophila compound eye
Author(s) -
NGERNSIRI LERTLUK,
FASCETTI NORA,
ROMRATANAPAN SUPPALUK,
BAUMGARTNER STEFAN
Publication year - 2006
Publication title -
insect science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 45
eISSN - 1744-7917
pISSN - 1672-9609
DOI - 10.1111/j.1744-7917.2006.00104.x
Subject(s) - ommatidium , biology , compound eye , eye development , microbiology and biotechnology , imaginal disc , morphogenesis , transmembrane protein , drosophila (subgenus) , gene , anatomy , genetics , drosophila melanogaster , phenotype , receptor , physics , optics
Ten‐a is one of the two Drosophila proteins that belong to the Ten M protein family. This protein is a type II transmembrane protein and is expressed mainly in the embryonic CNS, in the larval eye imaginal disc and in the compound eye of the pupa. Here, we investigate the role of ten‐a during development of the compound eye by using the Gal4/UAS system to induce ten‐a overexpression in the developing eye. We found that overexpression of ten‐a can perturb eye development during all stages examined. In an early stage, overexpression of ten‐a in eye primordial cells caused small and rough eyes and interfered with photoreceptor cell recruitment, resulting in some ommatidia having fewer or extra photoreceptor cells. Conversely, ten‐a overexpression during ommatidial formation caused severe eye defects due to absence of many cellular components. Interestingly, overexpression of ten‐a in the late stage developing ommatidial cluster affected the number of pigment cells, caused cone cells proliferation in many ommatidia, and caused some photoreceptor cell defects. These results suggest that ten‐a may be a novel gene required for normal eye morphogenesis.