Mitochondrial protein translocation-associated degradation

A comparative study of stress responses elicited by misfolded proteins targeted by bipartite or matrix-targeting signal sequences to yeast mitochondria

“…Subsequently, we found that deletion of small TOM components like Tom6, Tom7 and during stress which subsequently help to restore the cellular homeostasis [29][30][31] . Our model of IMS misfolding stress (imparted by bipartite signal sequence containing stressor proteins) would mimic the cellular response like mitoCPR especially during long standing chronic stress.…”

“…This clearly indicate the importance of TOM complex in the IMS misfolding stress. Recently, identification of various stress response pathways like mitochondrial compromised protein import response (mitoCPR)29 , mitochondrial translocase associated degradation (mitoTAD)30 have shown the importance of components TOM complex like Tom70 in recruiting various proteases like Msp1, Ubx2…”

Guarding the gate for mitochondrial entry

“…As a crucial part of the cellular machinery, disruption to their function could have serious consequences, and so mechanisms exist to combat mitochondrial dysfunction. On page 679, Mårtensson et al 1 report a pathway that tackles problems concerning the import of proteins into mitochondria, as they arise, to prevent mitochondrial and cellular dysfunction. This pathway uses part of the cellular repair kit that handles damaged proteins in another organelle -the endoplasmic reticulum (ER).…”

“…M any studies [1][2][3][4][5][6] in the past decade have shown that inter actions between tumour cells and nerve cells can influence the progression of various types of cancer. In prostate tumours, the presence of newly formed nerve cells is associated with the progression of malignancy and tumour spread to other locations in the body 1,2,7 . The microenvironment of a tumour can permit the development of such new nerve cells in a process called neo-neurogenesis.…”

The mitochondrial surface receptor Tom70 protects the cytosol against mitoprotein-induced stress

“…Mitochondrial protein biogenesis strictly depends on the cytosolic chaperone capacity (Becker et al, 1996;Ben-Menachem et al, 2018;Deshaies et al, 1988;Doring et al, 2017;Hoseini et al, 2016;Stein et al, 2019;Terada et al, 1996). Presumably as a consequence of their strong tendency to sequester chaperones, precursor proteins accumulating in the cytosol induce a sudden growth arrest, trigger the heat shock response to increase components of the chaperone and proteasome system, and activate specific factors on the mitochondrial surface that clean off translocation intermediates (Boos et al, 2019;Boos et al, 2020;Martensson et al, 2019;Shakya et al, 2020;Wang and Chen, 2015;Weidberg and Amon, 2018;Wrobel et al, 2015).…”