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Gene Review

Chi  -  Chip

Drosophila melanogaster

Synonyms: CG3924, CHIP, Dmel\CG3924, LDB, Ldb, ...
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High impact information on Chi

  • We show here that this communication is regulated by Osa, which is recruited by Pannier and Chip. Osa belongs to Brahma chromatin remodeling complexes and we show that Osa negatively regulates ac/sc [1].
  • Consequently, Pannier and Chip also play an essential role during repression of proneural gene expression [1].
  • Importantly, Chip also appears to have broad functions beyond interactions with LIM domain proteins [2].
  • Suhw bound to a gypsy insertion in the cut gene also appears to act interchromosomally to antagonize enhancer-promoter interactions on the homologous chromosome when activity of the Chip gene is reduced [2].
  • SEU encodes a plant-specific regulatory protein with sequence similarity in a conserved dimerization domain to the LIM-domain binding 1/Chip proteins in mouse and Drosophila [3].

Biological context of Chi

  • In support of this model, we show that the dLdb/Chip excess-of-function phenotypes can be rescued by ap overexpression [4].
  • Embryos without Chip activity lack segments and show abnormal gap and pair-rule gene expression, although no LIM domain proteins are known to regulate segmentation [2].
  • The Drosophila protein Chip potentiates activation by several enhancers and is required for embryonic segmentation [5].
  • We theorize that Mod(mdg4)-67.2 usually aids gene activation but can also act as a coinsulator by helping Su(Hw) trap facilitators of activation, such as the Chip protein [6].

Anatomical context of Chi

  • Within the Pannier domain of expression, Pannier and Apterous may compete for binding to their common Chip cofactor, and the accurate stoichiometry between these three proteins is essential for both proneural prepattern and compartmentalization of the thorax [7].

Physical interactions of Chi

  • We define the domains of Chip required for LIM-HD binding and for homodimerization and show that mutant proteins deleted for these domains act in a dominant-negative fashion to disrupt Ap function [8].

Other interactions of Chi

  • Here we report that dLdb/Chip encodes a LIM-binding cofactor that controls Ap activity [4].


  1. Enhancer-promoter communication mediated by Chip during Pannier-driven proneural patterning is regulated by Osa. Heitzler, P., Vanolst, L., Biryukova, I., Ramain, P. Genes Dev. (2003) [Pubmed]
  2. Chip, a widely expressed chromosomal protein required for segmentation and activity of a remote wing margin enhancer in Drosophila. Morcillo, P., Rosen, C., Baylies, M.K., Dorsett, D. Genes Dev. (1997) [Pubmed]
  3. Transcriptional repression of target genes by LEUNIG and SEUSS, two interacting regulatory proteins for Arabidopsis flower development. Sridhar, V.V., Surendrarao, A., Gonzalez, D., Conlan, R.S., Liu, Z. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  4. The relative expression amounts of apterous and its co-factor dLdb/Chip are critical for dorso-ventral compartmentalization in the Drosophila wing. Fernández-Fúnez, P., Lu, C.H., Rincón-Limas, D.E., García-Bellido, A., Botas, J. EMBO J. (1998) [Pubmed]
  5. Chip interacts with diverse homeodomain proteins and potentiates bicoid activity in vivo. Torigoi, E., Bennani-Baiti, I.M., Rosen, C., Gonzalez, K., Morcillo, P., Ptashne, M., Dorsett, D. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  6. Insulation of enhancer-promoter communication by a gypsy transposon insert in the Drosophila cut gene: cooperation between suppressor of hairy-wing and modifier of mdg4 proteins. Gause, M., Morcillo, P., Dorsett, D. Mol. Cell. Biol. (2001) [Pubmed]
  7. Interactions between chip and the achaete/scute-daughterless heterodimers are required for pannier-driven proneural patterning. Ramain, P., Khechumian, R., Khechumian, K., Arbogast, N., Ackermann, C., Heitzler, P. Mol. Cell (2000) [Pubmed]
  8. Chip and apterous physically interact to form a functional complex during Drosophila development. van Meyel, D.J., O'Keefe, D.D., Jurata, L.W., Thor, S., Gill, G.N., Thomas, J.B. Mol. Cell (1999) [Pubmed]
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