Yan Qing, Li Xiao-Ping, Tumer Nilgun E
Department of Plant Biology and Pathology, School of Environmental and Biological Sciences, Rutgers University, New Brunswick, New Jersey, United States of America.
PLoS One. 2014 Dec 1;9(12):e113719. doi: 10.1371/journal.pone.0113719. eCollection 2014.
Ricin A chain (RTA) undergoes retrograde trafficking and is postulated to use components of the endoplasmic reticulum (ER) associated degradation (ERAD) pathway to enter the cytosol to depurinate ribosomes. However, it is not known how RTA evades degradation by the proteasome after entry into the cytosol. We observed two distinct trafficking patterns among the precursor forms of wild type RTA and nontoxic variants tagged with enhanced green fluorescent protein (EGFP) at their C-termini in yeast. One group, which included wild type RTA, underwent ER-to-vacuole transport, while another group, which included the G83D variant, formed aggregates in the ER and was not transported to the vacuole. Peptide: N-glycanase (Png1), which catalyzes degradation of unfolded glycoproteins in the ERAD pathway affected depurination activity and toxicity of wild type RTA and G83D variant differently. PreG83D variant was deglycosylated by Png1 on the ER membrane, which reduced its depurination activity and toxicity by promoting its degradation. In contrast, wild type preRTA was deglycosylated by the free pool of Png1 in the cytosol, which increased its depurination activity, possibly by preventing its degradation. These results indicate that wild type RTA has a distinct requirement for Png1 compared to the G83D variant and is deglycosylated by Png1 in the cytosol as a possible strategy to avoid degradation by the ERAD pathway to reach the ribosome.
蓖麻毒素A链(RTA)进行逆向运输,并推测其利用内质网(ER)相关降解(ERAD)途径的组分进入细胞质以使核糖体脱嘌呤。然而,尚不清楚RTA进入细胞质后如何逃避蛋白酶体的降解。我们在酵母中观察到野生型RTA的前体形式和在其C末端标记有增强型绿色荧光蛋白(EGFP)的无毒变体之间的两种不同运输模式。一组包括野生型RTA,进行内质网到液泡的运输,而另一组包括G83D变体,在内质网中形成聚集体且未运输到液泡。肽:N-聚糖酶(Png1),其催化ERAD途径中未折叠糖蛋白的降解,对野生型RTA和G83D变体的脱嘌呤活性和毒性有不同影响。PreG83D变体在内质网膜上被Png1去糖基化,这通过促进其降解降低了其脱嘌呤活性和毒性。相反,野生型preRTA在细胞质中被Png1的游离池去糖基化,这可能通过防止其降解增加了其脱嘌呤活性。这些结果表明,与G83D变体相比,野生型RTA对Png1有不同的需求,并且在细胞质中被Png1去糖基化,这可能是一种避免被ERAD途径降解以到达核糖体的策略。