Reference Report

Reference
Citation	Kavlie, R.G., Kernan, M.J., Eberl, D.F. (2010). Hearing in Drosophila Requires TilB, a Conserved Protein Associated With Ciliary Motility. Genetics 185(1): 177--188. (Export to RIS)
FlyBase ID	FBrf0210892
Publication Type	Research paper
PubMed ID	20215474
PubMed Abstract	Cilia were present in the earliest eukaryotic ancestor and underlie many biological processes ranging from cell motility and propulsion of extracellular fluids to sensory physiology. We investigated the contribution of the touch insensitive larva B (tilB) gene to cilia function in Drosophila melanogaster. Mutants of tilB exhibit dysfunction in sperm flagella and ciliated dendrites of chordotonal organs that mediate hearing and larval touch sensitivity. Mutant sperm axonemes as well as sensory neuron dendrites of Johnston's organ, the fly's auditory organ, lack dynein arms. Through deficiency mapping and sequencing candidate genes, we identified tilB mutations in the annotated gene CG14620. A genomic CG14620 transgene rescued deafness and male sterility of tilB mutants. TilB is a 395-amino-acid protein with a conserved N-terminal leucine-rich repeat region at residues 16-164 and a coiled-coil domain at residues 171-191. A tilB-Gal4 transgene driving fluorescently tagged TilB proteins elicits cytoplasmic expression in embryonic chordotonal organs, in Johnston's organ, and in sperm flagella. TilB does not appear to affect tubulin polyglutamylation or polyglycylation. The phenotypes and expression of tilB indicate function in cilia construction or maintenance, but not in intraflagellar transport. This is also consistent with phylogenetic association of tilB homologs with presence of genes encoding axonemal dynein arm components. Further elucidation of tilB functional mechanisms will provide greater understanding of cilia function and will facilitate understanding ciliary diseases.
DOI	10.1534/genetics.110.114009
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Language of Publication	English
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Publication Type	Journal
Abbreviation	Genetics
Title	Genetics
Publication Year	1916-
ISBN/ISSN	0016-6731
Data from Reference
Aberrations (16)
	Df(1)16-2-13 Df(1)16-3-22 Df(1)17-25 Df(1)48-2 Df(1)C74 Df(1)DCB1-35c Df(1)GA22 Df(1)JC77 Df(1)LB6 Df(1)R20 Df(1)R21 Df(1)R35 Df(1)R38 Df(1)R44 Df(1)S54 Dp(1;Y)y²67g19.1
Alleles (15)
	Avic\GFP^Scer\UAS.cUa Scer\GAL4^elav.PU Scer\GAL4^tilB.PK T:Avic\GFP^EGFP T:Avic\GFP^YFP.Venus tilB¹ tilB² tilB^+t3.5 tilB^{CCTilBD.Scer\UAS.T:Avic\GFP-EGFP} tilB^{LRR.Scer\UAS.T:Hsap\MYC} tilB^{LRRCC.Scer\UAS.T:Hsap\MYC} tilB^{Scer\UAS.T:Avic\GFP-EGFP} tilB^{Scer\UAS.T:Avic\GFP-YFP.Venus} tilB^{Scer\UAS.T:Hsap\MYC} tilB^{TilBD.Scer\UAS.T:Avic\GFP-EGFP}
Constructs (11)
	P{elav-GAL4.U} P{tilB.3.5} P{tilB-Gal4.K} P{UAS-GFP.U} P{UASp-tilB.Venus} P{UAS-tilB.CCTilBD.EGFP} P{UAS-tilB.EGFP} P{UAS-tilB.LRR.Myc} P{UAS-tilB.LRRCC.Myc} P{UAS-tilB.Myc} P{UAS-tilB.TilBD.EGFP}
Genes (6)
	Avic\GFP CG14614 CG14615 Scer\GAL4 T:Hsap\MYC tilB
Natural transposons (1)
	P-element