BLISTERED - A GENE REQUIRED FOR VEIN INTERVEIN FORMATION IN WINGS OF DROSOPHILA/

Citation
D. Fristrom et al., BLISTERED - A GENE REQUIRED FOR VEIN INTERVEIN FORMATION IN WINGS OF DROSOPHILA/, Development, 120(9), 1994, pp. 2661-2671
Citations number
37
Categorie Soggetti
Developmental Biology
Journal title
ISSN journal
09501991
Volume
120
Issue
9
Year of publication
1994
Pages
2661 - 2671
Database
ISI
SICI code
0950-1991(1994)120:9<2661:B-AGRF>2.0.ZU;2-Z
Abstract
We have characterized the blistered (bs) locus phenotypically, genetic ally and developmentally using a set of new bs alleles. Mutant defects range from wings with ectopic veins and intervein blisters to complet ely ballooned wings where the distinction between vein and intervein i s lost. Mosaic analyses show that severe bs alleles behave largely aut onomously; homozygous patches having vein-like properties. Development al analyses were undertaken using light and electron microscopy of wil d-type and bs wings as well as confocal microscopy of phalloidin- and laminin-stained preparations. bs defects were first seen early in the prepupal period with the failure of apposition of dorsal and ventral w ing epithelia. Correspondingly, during definitive vein/intervein diffe rentiation in the pupal period (18-36 hours after puparium formation), the extent of dorsal/ventral reapposition is reduced in bs wings. Reg ions of the wing that fail to become apposed differentiate properties of vein cells; i.e. become constricted apically and acquire a laminin- containing matrix basally. To further understand bs function, we exami ned genetic interactions between various bs alleles and mutants of two genes whose products have known functions in wing development. (i) rh omboid, a component of the EGF-R signalling pathway, is expressed in v ein cells and is required for specification of vein cell fate. rho(ve) mutations (lacking rhomboid in wings) suppress the excess vein format ion and associated with bs. Conversely, rho expression in prepupal and pupal bs wings is expanded in the regions of increased vein formation . (ii) The integrin genes, inflated and myospheroid, are expressed in intervein cells and are required for adhesion between the dorsal and v entral wing surfaces. Loss of integrin function results in intervein b listers. Integrin mutants interact with bs mutants to increase the fre quency of intervein blisters but do not typically enhance vein defects . Both developmental and genetic analyses suggest that the bs product is required during metamorphosis for the initiation of intervein devel opment and the concomitant inhibition of vein development.