Fig. 9: Schematic model depicting the MQC pathway triggered by ablation of ATOM69 in trypanosomes. | Nature Communications

Fig. 9: Schematic model depicting the MQC pathway triggered by ablation of ATOM69 in trypanosomes.

From: Mistargeting of aggregation prone mitochondrial proteins activates a nucleus-mediated posttranscriptional quality control pathway in trypanosomes

Fig. 9

Ablation of atypical translocase of the outer membrane 69 (ATOM69) results in cytosolic accumulation of primarily hydrophobic proteins which triggers a quality control pathway that ultimately leads to the degradation of the mislocalised hydrophobic proteins. The pathway requires nuclear release of the ubiquitin-like protein 1, TbUbL1, the main subject of the present study (yellow). Moreover, TbUbL1, the ubiquitin ligase TbE3HECT1 (red), Tb927.9.7200 (not shown) and the proteasome (red) are recruited from the cytosol to the mitochondrion. The role of TbE3HECT1 may be to ubiquitinate the mislocalised hydrophobic proteins which subsequently may be recognised by TbUbL1 and transferred to the proteasome.

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