Journal articles
The SLX4 Complex Is a SUMO E3 Ligase that Impacts on Replication Stress Outcome and Genome Stability
Abstract : The SLX4 Fanconi anemia protein is a tumor suppres- sor that may act as a key regulator that engages the cell into specific genome maintenance pathways. Here, we show that the SLX4 complex is a SUMO E3 ligase that SUMOylates SLX4 itself and the XPF sub- unit of the DNA repair/recombination XPF-ERCC1 endonuclease. This SLX4-dependent activity is medi- ated by a remarkably specific interaction between SLX4 and the SUMO-charged E2 conjugating enzyme UBC9 and relies not only on newly identified SUMO- interacting motifs (SIMs) in SLX4 but also on its BTB domain. In contrast to its ubiquitin-binding UBZ4 motifs, SLX4 SIMs are dispensable for its DNA inter- strand crosslink repair functions. Instead, while detri- mental in response to global replication stress, the SUMO E3 ligase activity of the SLX4 complex is crit- ical to prevent mitotic catastrophe following common fragile site expression.
Cited literature [47 references]
https://hal-amu.archives-ouvertes.fr/hal-01429041
Contributor : Pierre-Henri Gaillard <>
Submitted on : Friday, January 6, 2017 - 5:31:43 PM
Last modification on : Monday, December 21, 2020 - 4:20:03 PM
Long-term archiving on: : Friday, April 7, 2017 - 6:01:29 PM
Contributor : Pierre-Henri Gaillard <>
Submitted on : Friday, January 6, 2017 - 5:31:43 PM
Last modification on : Monday, December 21, 2020 - 4:20:03 PM
Long-term archiving on: : Friday, April 7, 2017 - 6:01:29 PM
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