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The “SnapShot from Cell Press: Mitochondrial Dynamics” poster describes the mitochondrial fusion-division cycle, specifically the mammalian and yeast fusion machinery and the division machinery in mammals, yeast and algae.
The poster highlights the importance of an intact mitochondrial fusion-division cycle, demonstrating how alterations result in neurodegenerative diseases, such as Parkinson’s, and neuropathies, such as Charcot-Marie-Tooth type 2A. Mutations in the mitofusion proteins and GTPases, Mfn1 and Mfn2 are primarily responsible for the development of Charcot-Marie-Tooth type 2A disease in mammals. Autosomal dominant optic atrophy type 1 on the other hand is caused by mutations in Opa1 (a dynamin related GTPase), while mutations in GDAP1 (Ganglioside-induced differentiation-associated protein 1) result in Charcot-Marie-Tooth type 4A disease.
Aberrant ubiquitination patterns, especially when caused by mutations in the Parkin RING-finger E3 ubiquitin ligase, play a critical role in a variety of neurodegenerative diseases (Chan et al. 2011). Parkin, as the name implies, is associated with the development of Parkinson’s disease. Accordingly, it mediates the “degradation of dysfunctional mitochondria by autophagy” through K-48 mediated ubiquitination (Chan et al. 2011). Parkin substrates include Mfn1 and Mfn2 as well as apoptosis related proteins such as Bak and Bax (Chan et al. 2011, Johnson et al. 2012).
In order to make it easier for you to select reagents for mitochondrial dynamics research, we have grouped antibodies against the critical proteins mentioned on the poster in a convenient selector tool. These include our range of anti-ubiquitin antibodies that enable you to distinguish between free ubiquitin and mono- and polyubiquitinated proteins.
Chan NC et al. (2011). Broad activation of the ubiquitin-proteasome system by Parkin is critical for mitophagy. Human Molecular Genetics 1:20(9):1726-37.
Johnson BN (2012). The ubiquitin E3 ligase parkin regulates the proapoptotic function of Bax. Proceedings of the Natural Academy Sciences 17:109 (16):6283-8.