Fu Weimin, Sun Joanne, Huang Guochang, Liu Jeffrey C, Kaufman Andrew, Ryan Russell J H, Ramanathan Suresh Y, Venkatesh Tadmiri, Singh Bhuvanesh
From the Department of Surgery, Laboratory of Epithelial Cancer Biology, Memorial Sloan Kettering Cancer Center, New York, New York 10065 and.
Department of Biology, The City College of New York, New York, New York 10031.
J Biol Chem. 2016 Mar 18;291(12):6200-17. doi: 10.1074/jbc.M115.692756. Epub 2016 Jan 20.
SCCRO (squamous cell carcinoma-related oncogene; also known as DCUN1D1) is a highly conserved gene that functions as an E3 in neddylation. Although inactivation of SCCRO in yeast results in lethality, SCCRO(-/-) mice are viable. The exclusive presence of highly conserved paralogues in higher organisms led us to assess whether compensation by SCCRO paralogues rescues lethality in SCCRO(-/-) mice. Using murine and Drosophila models, we assessed the in vivo activities of SCCRO and its paralogues in cullin neddylation. We found that SCCRO family members have overlapping and antagonistic activity that regulates neddylation and cell proliferation activities in vivo. In flies, both dSCCRO and dSCCRO3 promote neddylation and cell proliferation, whereas dSCCRO4 negatively regulates these processes. Analysis of somatic clones showed that the effects that these paralogues have on proliferation serve to promote cell competition, leading to apoptosis in clones with a net decrease in neddylation activity. We found that dSCCRO and, to a lesser extent, dSCCRO3 rescue the neddylation and proliferation defects promoted by expression of SCCRO4. dSCCRO and dSCCRO3 functioned cooperatively, with their coexpression resulting in an increase in both the neddylated cullin fraction and proliferation activity. In contrast, human SCCRO and SCCRO4 promote, and human SCCRO3 inhibits, neddylation and proliferation when expressed in flies. Our findings provide the first insights into the mechanisms through which SCCRO family members cooperatively regulate neddylation and cell proliferation.
SCCRO(鳞状细胞癌相关癌基因;也称为DCUN1D1)是一种高度保守的基因,在NEDD化过程中作为E3发挥作用。尽管酵母中SCCRO的失活会导致致死性,但SCCRO(-/-)小鼠是存活的。高等生物中高度保守的旁系同源物的独特存在促使我们评估SCCRO旁系同源物的补偿作用是否能挽救SCCRO(-/-)小鼠的致死性。我们使用小鼠和果蝇模型,评估了SCCRO及其旁系同源物在cullin NEDD化中的体内活性。我们发现SCCRO家族成员具有重叠和拮抗活性,在体内调节NEDD化和细胞增殖活性。在果蝇中,dSCCRO和dSCCRO3都促进NEDD化和细胞增殖,而dSCCRO4则对这些过程起负调节作用。体细胞克隆分析表明,这些旁系同源物对增殖的影响有助于促进细胞竞争,导致NEDD化活性净降低的克隆发生凋亡。我们发现dSCCRO以及程度较轻的dSCCRO3可挽救由SCCRO4表达所促进的NEDD化和增殖缺陷。dSCCRO和dSCCRO3协同发挥作用,它们的共表达导致NEDD化的cullin部分和增殖活性均增加。相比之下,人类SCCRO和SCCRO4在果蝇中表达时促进NEDD化和增殖,而人类SCCRO3则抑制NEDD化和增殖。我们的研究结果首次揭示了SCCRO家族成员协同调节NEDD化和细胞增殖的机制。