Literature DB >> 2693466

Expression in Escherichia coli of fragments of glial fibrillary acidic protein: characterization, assembly properties and paracrystal formation.

R A Quinlan1, R D Moir, M Stewart.   

Abstract

We have expressed in Escherichia coli a 1258 bp cDNA fragment corresponding to 97% of mouse glial fibrillary acidic protein (GFAP), the principal intermediate filament protein of astrocytes. High levels of expression were obtained, as a fusion protein with 32 residues of the bacteriophage lambda cII protein, using the pLcII expression vector system of K. Nagai and H.-C. Thogersen. Although removal of the cII protein fragment by proteolysis using factor X proved difficult, a protein corresponding to most of the cDNA fragment was obtained by cleaving at the endogenous thrombin site near the middle of the N-terminal non-helical domain of GFAP. A shorter 1047 bp fragment, in which the C-terminal non-helical domain of GFAP was deleted, was also produced using oligonucleotide-directed site-specific mutagenesis of the original cDNA clone. After proteolysis with thrombin, this material gave a fragment that corresponded to the alpha-helical coiled-coil rod region of the GFAP molecule, together with a portion of the non-helical N-terminal domain. The fragments produced were characterized both biochemically and ultrastructurally, and appeared to retain the conformation of native GFAP. Crosslinking showed that all fragments formed molecules containing two chains ('dimers') that associated to form four-chain molecular dimers ('tetramers') analogous to those formed by intact intermediate filament proteins. Shadowed preparations showed the presence of rod-like particles that closely resembled those observed for other intermediate filament proteins and proteolytically prepared rod domains. Remarkably, the fusion protein produced from the entire 1258 bp cDNA fragment and the cII peptide was able to form filaments that closely resembled those produced by native GFAP. However, fragments in which either the cII peptide or the C-terminal non-helical domain were removed, or in which both were removed, failed to form filaments under standard assembly conditions. Although preliminary in nature, these results suggest that both N- and C-terminal non-helical domains may have a role in intermediate filament formation. Moreover, the fragment corresponding approximately to the GFAP rod formed paracrystals similar to those observed with other coiled-coil proteins. The molecules in these paracrystals were arranged antiparallel with the two molecules in the unit cell, which may correspond to the four-chain molecular dimer (tetramer), overlapping by approximately two-thirds of their length.

Entities:  

Mesh:

Substances:

Year:  1989        PMID: 2693466     DOI: 10.1242/jcs.93.1.71

Source DB:  PubMed          Journal:  J Cell Sci        ISSN: 0021-9533            Impact factor:   5.285


  19 in total

1.  Alexander disease causing mutations in the C-terminal domain of GFAP are deleterious both to assembly and network formation with the potential to both activate caspase 3 and decrease cell viability.

Authors:  Yi-Song Chen; Suh-Ciuan Lim; Mei-Hsuan Chen; Roy A Quinlan; Ming-Der Perng
Journal:  Exp Cell Res       Date:  2011-07-02       Impact factor: 3.905

2.  Truncation of alphaB-crystallin by the myopathy-causing Q151X mutation significantly destabilizes the protein leading to aggregate formation in transfected cells.

Authors:  Victoria H Hayes; Glyn Devlin; Roy A Quinlan
Journal:  J Biol Chem       Date:  2008-01-29       Impact factor: 5.157

3.  Identification of a novel nonsense mutation in the rod domain of GFAP that is associated with Alexander disease.

Authors:  Tai-Seung Nam; Jin Hee Kim; Chi-Hsuan Chang; Woong Yoon; Yoon Seok Jung; Sa-Yoon Kang; Boo Ahn Shin; Ming-Der Perng; Seok-Yong Choi; Myeong-Kyu Kim
Journal:  Eur J Hum Genet       Date:  2014-04-23       Impact factor: 4.246

4.  Purification and characterization of the bacteriophage P4 delta protein.

Authors:  B Julien; R Calendar
Journal:  J Bacteriol       Date:  1995-07       Impact factor: 3.490

5.  The N-terminal peptide of mammalian GTP cyclohydrolase I is an autoinhibitory control element and contributes to binding the allosteric regulatory protein GFRP.

Authors:  Christina E Higgins; Steven S Gross
Journal:  J Biol Chem       Date:  2010-12-16       Impact factor: 5.157

6.  Overexpression of bacterio-opsin in Escherichia coli as a water-soluble fusion to maltose binding protein: efficient regeneration of the fusion protein and selective cleavage with trypsin.

Authors:  G Q Chen; J E Gouaux
Journal:  Protein Sci       Date:  1996-03       Impact factor: 6.725

7.  Expression of soluble, biologically active recombinant human tumstatin in Escherichia coli.

Authors:  Yi-Qin Luo; Liang-Hua Wang; Qui Yi; Bing-Hua Jiao
Journal:  Clin Exp Med       Date:  2008-04-03       Impact factor: 3.984

Review 8.  Insights into the beaded filament of the eye lens.

Authors:  Ming-Der Perng; Qingjiong Zhang; Roy A Quinlan
Journal:  Exp Cell Res       Date:  2007-04-06       Impact factor: 3.905

9.  Glial fibrillary acidic protein filaments can tolerate the incorporation of assembly-compromised GFAP-delta, but with consequences for filament organization and alphaB-crystallin association.

Authors:  Ming-Der Perng; Shu-Fang Wen; Terry Gibbon; Jinte Middeldorp; Jacqueline Sluijs; Elly M Hol; Roy A Quinlan
Journal:  Mol Biol Cell       Date:  2008-08-06       Impact factor: 4.138

10.  The specificity of the interaction between αB-crystallin and desmin filaments and its impact on filament aggregation and cell viability.

Authors:  Jayne L Elliott; Ming Der Perng; Alan R Prescott; Karin A Jansen; Gijsje H Koenderink; Roy A Quinlan
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  2013-03-25       Impact factor: 6.237

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.