A dominant negative allele of the Drosophila leucine zipper protein bunched blocks bunched function during tissue patterning

被引:2
作者
Ash, David M. [1 ]
Hackney, Jennifer F. [1 ]
Jean-Francois, Michele [1 ]
Burton, Neal C. [1 ]
Doberis, Leonard L. [1 ]
机构
[1] Univ Missouri, Sch Biol Sci, Div Mol Biol & Biochem, Kansas City, MO 64110 USA
基金
美国国家科学基金会;
关键词
tissue patterning; dominant negative; TSC-22/GILZ family; bunched; GILZ; TSC-22; oogenesis; Drosophila;
D O I
10.1016/j.mod.2007.05.003
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The bunched (bun) gene encodes the Drosophila member of the TSC-22/GILZ family of leucine zipper transcriptional regulators. The bun locus encodes multiple BUN protein isoforms and has diverse roles during patterning of the eye, wing margin, dorsal notum and eggshell. Here we report the construction and activity of a dominant negative allele (BunDN) of the BUN-B isoform. In the ovary, BunDN expression in the follicle cells (FC) resulted in epithelial defects including aberrant accumulation of DE-cadherin and failure to rearrange into columnar FC cell shapes. BunDN expression in the posterior FC led to loss of epithelial integrity associated with extensive apoptosis. BunDN FC phenotypes collectively resemble loss-of-function bun mutant phenotypes. BunDN expression using tissue-specific imaginal disk drivers resulted in characteristic cuticular patterning defects that were enhanced by bun mutations and suppressed by co-expression of the BUN-B protein isoform. These data indicate that BunDN has dominant negative activity useful to identify bun functions and genetic interactions that occur during tissue patterning. (c) 2007 Published by Elsevier Ireland Ltd.
引用
收藏
页码:559 / 569
页数:11
相关论文
共 62 条
[21]  
Fleming RJ, 1997, DEVELOPMENT, V124, P2973
[22]   A SAGE approach to discovery of genes involved in autophagic cell death [J].
Gorski, SM ;
Chittaranjan, S ;
Pleasance, ED ;
Freeman, JD ;
Anderson, CL ;
Varhol, RJ ;
Coughlin, SM ;
Zuyderduyn, SD ;
Jones, SJM ;
Marra, MA .
CURRENT BIOLOGY, 2003, 13 (04) :358-363
[23]   Peroxisome proliferator-activated receptor γ and transforming growth factor-β pathways inhibit intestinal epithelial cell growth by regulating levels of TSC-22 [J].
Gupta, RA ;
Sarraf, P ;
Brockman, JA ;
Shappell, SB ;
Raftery, LA ;
Willson, TM ;
DuBois, RN .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (09) :7431-7438
[24]  
Haerry TE, 1998, DEVELOPMENT, V125, P3977
[25]   CLONING OF RAT SERTOLI-CELL FOLLICLE-STIMULATING-HORMONE PRIMARY RESPONSE COMPLEMENTARY DEOXYRIBONUCLEIC-ACID - REGULATION OF TSC-22 GENE-EXPRESSION [J].
HAMIL, KG ;
HALL, SH .
ENDOCRINOLOGY, 1994, 134 (03) :1205-1212
[26]  
Hashiguchi A, 2004, DEV GROWTH DIFFER, V46, P535
[27]  
HAY BA, 1994, DEVELOPMENT, V120, P2121
[28]  
Heitzler P, 1996, GENETICS, V143, P1271
[29]   Cytoplasmic TSC-22 (transforming growth factor-β-stimulated clone-22) markedly enhances the radiation sensitivity of salivary gland cancer cells [J].
Hino, S ;
Kawamata, H ;
Omotehara, F ;
Uchida, D ;
Miwa, Y ;
Begum, NM ;
Yoshida, H ;
Sato, M ;
Fujimori, T .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2002, 292 (04) :957-963
[30]   Unique patterns of gene expression changes in liver after treatment of mice for 2 weeks with different known carcinogens and non-carcinogens [J].
Iida, M ;
Anna, CH ;
Holliday, WM ;
Collins, JB ;
Cunningham, ML ;
Sills, RC ;
Devereux, TR .
CARCINOGENESIS, 2005, 26 (03) :689-699