Wei Jiajie, Gibbs James S, Hickman Heather D, Cush Stephanie S, Bennink Jack R, Yewdell Jonathan W
From the Laboratory of Viral Diseases, NIAID, National Institutes of Health, Bethesda, Maryland 20892.
From the Laboratory of Viral Diseases, NIAID, National Institutes of Health, Bethesda, Maryland 20892
J Biol Chem. 2015 Jun 26;290(26):16431-9. doi: 10.1074/jbc.M115.658062. Epub 2015 May 13.
Green fluorescent protein (GFP) and other fluorescent proteins are essential tools for biological research. When fused to peptides or proteins as a reporter, GFP enables localization and quantitation of gene products in otherwise unmanipulated live cells or organisms. We previously reported that a sizable fraction of nascent GFP is post-translationally converted into a 20-kDa Triton X-100-insoluble proteasome substrate (Qian, S. B., Princiotta, M. F., Bennink, J. R., and Yewdell, J. W. (2006) J. Biol. Chem. 281, 392-400; Dolan, B. P., Li, L., Veltri, C. A., Ireland, C. M., Bennink, J. R., and Yewdell, J. W. (2011) J. Immunol. 186, 2065-2072). Here, we show that a similarly sized fragment is generated by all GFP and red fluorescent protein family members we examined. We demonstrate that fragmentation is a by-product of GFP chromophore rearrangement. A non-rearranging GFP mutant fails to fragment and generates diminished levels of K(b)-SIINFEKL complexes when SIINFEKL is genetically fused to either the C- or N-terminal domains of GFP fusion proteins. Instructively, another fragmenting GFP mutant that cannot create the functional chromophore but still generates fragments also demonstrates diminished K(b)-SIINFEKL generation. However, the mutant and wild-type fragments differ fundamentally in that wild-type fragments are rapidly liberated from the intact molecule and degraded quickly, accounting for increased K(b)-SIINFEKL generation. In the fragmenting mutant, the fragments are generated slowly and remain associated, likely in a native conformation based on their original structural description (Barondeau, D. P., Kassmann, C. J., Tainer, J. A., and Getzoff, E. D. (2006) J. Am. Chem. Soc. 128, 4685-4693). The wild-type GFP fragments represent the first biochemically defined natural defective ribosomal products to contribute peptides for immunosurveillance, enabling quantitation of peptide generation efficiency from this source of defective ribosomal products. More broadly, given the wide use of fluorescent proteins, their ubiquitous and abundant fragmentation must be considered when interpreting experiments using these extremely useful probes.
绿色荧光蛋白(GFP)及其他荧光蛋白是生物学研究的重要工具。当作为报告基因与肽或蛋白质融合时,GFP能够在未经处理的活细胞或生物体中对基因产物进行定位和定量。我们之前报道过,相当一部分新生GFP会在翻译后转化为一种20 kDa的Triton X - 100不溶性蛋白酶体底物(钱,S. B.,普林乔塔,M. F.,本宁克,J. R.,以及尤德尔,J. W.(2006年)《生物化学杂志》281卷,392 - 400页;多兰,B. P.,李,L.,韦尔特里,C. A.,爱尔兰,C. M.,本宁克,J. R.,以及尤德尔,J. W.(2011年)《免疫学杂志》186卷,2065 - 2072页)。在此,我们表明我们所检测的所有GFP和红色荧光蛋白家族成员都会产生类似大小的片段。我们证明片段化是GFP发色团重排的副产物。一个不发生重排的GFP突变体不会产生片段,并且当SIINFEKL基因融合到GFP融合蛋白的C端或N端结构域时,K(b)-SIINFEKL复合物的水平会降低。具有启发性的是,另一个不能形成功能性发色团但仍会产生片段的片段化GFP突变体也显示出K(b)-SIINFEKL生成减少。然而,该突变体片段与野生型片段在根本上有所不同,即野生型片段会迅速从完整分子中释放并快速降解,这导致K(b)-SIINFEKL生成增加。在片段化突变体中,片段生成缓慢且保持关联,基于其原始结构描述(巴龙多,D. P.,卡斯曼,C. J.,泰纳,J. A.,以及格茨奥夫,E. D.(2006年)《美国化学会志》128卷,4685 - 4693页),可能处于天然构象。野生型GFP片段代表了首个经过生物化学定义的天然缺陷核糖体产物,可为免疫监视贡献肽段,从而能够定量从这种缺陷核糖体产物来源产生肽段的效率。更广泛地说,鉴于荧光蛋白的广泛应用,在解释使用这些极其有用的探针所进行的实验时,必须考虑它们普遍且大量的片段化现象。