Characterization of a new SUMO-1 nuclear body (SNB) enriched in pCREB, CBP, c-Jun in neuron-like UR61 cells

• Published in: Chromosoma 2007-10, Vol.116 (5), p.441-451
• Main Authors: Navascués, Joaquín, Bengoechea, Rocio, Tapia, Olga, Vaqué, José P, Lafarga, Miguel, Berciano, Maria T
• Format: Article
• Language: English
• Subjects: Animals; Axonogenesis; c-Jun protein; Cajal bodies; Cell differentiation; Cell Nucleolus - metabolism; Cell Nucleolus - ultrastructure; Cell survival; Cells, Cultured; CREB-Binding Protein - metabolism; Cyclic AMP response element-binding protein; Dexamethasone; Electron microscopy; Gene Expression Regulation; Glucocorticoids; JNK Mitogen-Activated Protein Kinases - metabolism; Neurons - chemistry; Neurons - metabolism; Neuroprotection; PC12 Cells; PML protein; Promyeloid leukemia; Proteins; Rats; Splicing factors; SUMO protein; SUMO-1 Protein - chemistry; SUMO-1 Protein - isolation & purification; SUMO-1 Protein - metabolism; Transcription; Transcription factors; Transfection; Ubiquitin
• ISSN: 0009-5915; 1432-0886
• DOI: 10.1007/s00412-007-0107-7

The neuron-like UR61 cell is a stable PC12 subline that contains a mouse N-ras oncogene. Dexamethasone (Dex) treatment induces a neuron-like differentiation, which is associated with neuritogenesis and nuclear expression of the glucocorticoid receptor and c-Jun. In differentiated UR61 cells, small ubiquitin-like modifiers 1 (SUMO-1) is concentrated in a new category of SUMO-1 nuclear bodies (SNBs) distinct from promyelocytic leukemia (PML) bodies by their large size and absence of PML protein. SNBs are 1 to 3 μm in diameter and exhibit a fine granular texture by electron microscopy. They are free of splicing factors and transcription foci and show spatial associations with Cajal bodies. In addition to SUMO-1 and the E2-conjugating enzyme Ubc9, which is essential for sumoylation, SNBs concentrate the transcriptional regulators CBP, CREB, and c-Jun. Moreover, transfection experiments demonstrate that SNBs accumulate the active conjugating form of SUMO-1 but not the conjugation defective variant of SUMO-1, supporting that SNBs are sites of sumoylation. Our results suggest that SNBs play a role in the control of the nucleoplasmic concentration of transcription regulators involved in neuroprotection and survival of the UR61 cells.