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Full-Text Articles in Biology
Does Vdac2 Have A Bh3 Domain?, Lillian Ferkany
Does Vdac2 Have A Bh3 Domain?, Lillian Ferkany
Honors Theses
Mitochondrial outer membrane permeabilization (MOMP) by Bax oligomerization triggers apoptosis. BCl-2 family proteins, classified as BH3 only proteins, pro-survival proteins, or pro-apoptotic proteins, control apoptosis partly through their agonist or antagonistic effects on Bax, which are mediated by their conserved BH3 domains. All BH3 domains form an alpha helix containing 5-7 conserved hydrophobic residues, designated H0-H5, and one conserved aspartic acid that drive interaction with Bax and other ‘multi-domain’ BCl-2 members. BH3 agonists induce Bax oligomerization, while BH3 antagonists sequester Bax to prevent MOMP. We discovered that voltage dependent anion channels (VDACs) in the MOM contain a putative BH3-like domain …
Myo19 Tethers Mitochondria To Endoplasmic Reticulum-Associated Actin To Promote Mitochondrial Fission, Stephen M. Coscia, Cameron P. Thompson, Qing Tang, Elana E. Baltrusaitis, Joseph A. Rhodenhiser, Omar A. Quintero, E. Michael Ostap, Melike Lakadamyali, Erika L. Holzbaur
Myo19 Tethers Mitochondria To Endoplasmic Reticulum-Associated Actin To Promote Mitochondrial Fission, Stephen M. Coscia, Cameron P. Thompson, Qing Tang, Elana E. Baltrusaitis, Joseph A. Rhodenhiser, Omar A. Quintero, E. Michael Ostap, Melike Lakadamyali, Erika L. Holzbaur
Biology Faculty Publications
Mitochondrial homeostasis requires a dynamic balance of fission and fusion. The actin cytoskeleton promotes fission, and we found that the mitochondrially localized myosin, myosin 19 (Myo19), is integral to this process. Myo19 knockdown induced mitochondrial elongation, whereas Myo19 overexpression induced fragmentation. This mitochondrial fragmentation was blocked by a Myo19 mutation predicted to inhibit ATPase activity and strong actin binding but not by mutations predicted to affect the working stroke of the motor that preserve ATPase activity. Super-resolution imaging indicated a dispersed localization of Myo19 on mitochondria, which we found to be dependent on metaxins. These observations suggest that Myo19 acts …