Format:
Online-Ressource
ISSN:
1460-2075
Content:
The LIM homeodomain (LIM‐HD) protein Apterous (Ap) and its cofactor DLDB/CHIP control dorso‐ ventral (D/V) patterning and growth of Drosophila wing. To investigate the molecular mechanisms of Ap/CHIP function we altered their relative levels of expression and generated mutants in the LIM1, LIM2 and HD domains of Ap, as well as in the LIM‐interacting and self‐association domains of CHIP. Using in vitro and in vivo assays we found that: (i) the levels of CHIP relative to Ap control D/V patterning; (ii) the LIM1 and LIM2 domains differ in their contributions to Ap function; (iii) Ap HD mutations cause weak dominant negative effects; (iv) overexpression of ChipΔSAD mutants mimics Ap lack‐of‐function, and this dominant negative phenotype is caused by titration of Ap because it can be rescued by adding extra Ap; and (v) overexpression of ChipΔLID mutants also causes an Ap lack‐of‐function phenotype, but it cannot be rescued by extra Ap. These results support the model that the Ap–CHIP active complex in vivo is a tetramer.
In:
volume:19
In:
number:11
In:
year:2000
In:
pages:2602-2614
In:
extent:13
In:
European Molecular Biology Organization, The EMBO journal, Heidelberg : EMBO Press, 1982-, 19, Heft 11 (2000), 2602-2614 (gesamt 13), 1460-2075
Language:
English
DOI:
10.1093/emboj/19.11.2602
URN:
urn:nbn:de:101:1-2023110104083277091421
URL:
https://doi.org/10.1093/emboj/19.11.2602
URL:
https://nbn-resolving.org/urn:nbn:de:101:1-2023110104083277091421
URL:
https://d-nb.info/1308124422/34
URL:
https://doi.org/10.1093/emboj/19.11.2602
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