HDAC6 controls autophagosome maturation essential for ubiquitin‐selective quality‐control autophagy

By Joo-Yong Lee, H. Koga, Y. Kawaguchi, Waixing Tang, Esther Wong, Ya‐sheng Gao, U. Pandey, Susmita Kaushik, Emily Tresse, Jianrong Lu and 3 more. EMBO Journal, 2010

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TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. (2010, background): “Genetic ablation of HDAC6 resulted in ubiquitinated protein aggregate accumulation and neurodegeneration in Drosophila and in mice (256).”
p62 links the autophagy pathway and the ubiqutin–proteasome system upon ubiquitinated protein degradation (2016, positive): “HDAC6 knockdown leads to failure of fusion between the autophagosome and lysosome and subsequent protein aggregation [86].”
Cellular strategies for controlling protein aggregation (2010, background): “Interestingly, one of the main players of aggresome formation, HDAC6, also controls a step that is essential for aggregate turnover by autophagy; the fusion of autophagosomes with lysosomes by the recruitment of the actin-remodelling machinery that is involved in this proces”
HDACs and HDAC Inhibitors in Cancer Development and Therapy (2016, positive): “The parkinmediated mitochondrial ubiquitination recruits HDAC6 and p62, which assemble the autophagy machinery and lead to mitochondrial clearance (Lee et al. 2010b).”
Septins: the fourth component of the cytoskeleton (2012, background): “, and actin has been found to promote the fusion of autophagosomes to lysosome”
Autophagy and aging. (2011, background): “This is linked to ageassociated pathologies, including triglyceride accumulation, mitochondrial dysfunction, muscle degeneration, and cardiac malfunction (Lee et al., 2010a).”