The Ubiquitin Ligase Smurf1 Functions in Selective Autophagy of Mycobacterium tuberculosis and Anti-tuberculous Host Defense

Abstract

A reader brought errors in Figure 4 to the authors' attention. In Figures 4A and 4D, several immunofluorescence panels were inadvertently reversed during their final arrangement. Panels that should have indicated the merge image were incorrectly placed where the single channel GFP image should be, and vice versa. Figures 4A and 4D have now been corrected online. The original results and conclusions are unaffected by these corrections. The authors accept responsibility for not detecting these errors prior to publication and regret any inconvenience this has caused.

Actin‐based motility allows Listeria monocytogenes to avoid autophagy in the macrophage cytosol

“…For example, markers involved in autophagy also recruit interferon-regulated GTPases known to promote lysis of pathogen-containing vacuoles and cytosolic microbes (Mitchell and Isberg, 2017). In addition, ubiquitylated proteins mediate the recruitment of the proteasome to cytosolic Salmonella enterica serovar Typhimurium ( S. Typhimurium) (Perrin et al , 2004) and Mycobacterium tuberculosis -associated structures (Franco et al , 2017). However, the molecular mechanisms and exact consequences of this recruitment remain to be determined.…”

“…The identification of ubiquitin ligases that selectively mark microbial pathogens will constitute one step towards delineating the unique features of antimicrobial autophagy and host cell-autonomous defense mechanisms. Ubiquitin ligases that target cytosolic S. Typhimurium (Huett et al , 2012; Noad et al , 2017; van Wijk et al , 2017) and M. tuberculosis -containing vacuoles (Franco et al , 2017; Manzanillo et al , 2013) have already been identified, but their spectrum of action remains to be further studied and their host or bacterial substrates are unknown. Importantly, microbial substrates for ubiquitylation might represent excellent targets for the development of antimicrobials and vaccines, since the immune system usually recognizes conserved microbial molecular patterns.…”

Emerging roles of HECT‐type E3 ubiquitin ligases in autophagy regulation

“…SMURFs also localize to the ER (Guo et al ., ). They are not required for general autophagy, but are regulators of selective autophagy, including xenophagy and mitophagy (Table ) (Borroni et al ., ; Franco et al .,; Orvedahl et al ., ).…”

Genetic control of autophagy underlies pathogenesis of inflammatory bowel disease

“…Ubiquitination plays a key role in bacterial targeting and a role has recently been emerging for specific E3 ligases in modulating substrate specificity in the autophagy pathway 71, 72 . Several E3 ubiquitin ligases including LRSAM1, Parkin, Smurf1, RNF166, and some TRIM proteins have each been shown to ubiquitinate bacteria or bacteria-associated proteins to drive antibacterial autophagy 73–76 . Various TRIM proteins have also been implicated in antibacterial autophagy as well as other types of selective autophagy that have a direct effect on inflammation 74, 77, 78 .…”

“…The E3 ubiquitin ligase Parkin is critical for mitophagy and has recently been shown to be recruited to intracellular M. tuberculosis and S. Typhimurium to promote autophagy 54, 74, 85 . The E3 ligase SMURF1 and the peroxisomal protein PEX13 are also critical for mitophagy, virophagy, and antibacterial autophagy 76, 86, 87 . The kinase TBK1 has been also recently been shown to be actively recruited to bacteria and damaged mitochondria; once there, TBK1-dependent phosphorylation recruits downstream adaptors required for antibacterial autophagy and mitophagy 53, 69 .…”