. Author manuscript; available in PMC: 2016 Apr 1.

Published in final edited form as: Curr Opin Cell Biol. 2014 Dec 23;33:74–81. doi: 10.1016/j.ceb.2014.12.003

Table 1.

UPR^mt inducing manipulations

	Genetic	Pharmacological
protein damage	aggregation prone OTC-Δ [20,22], EndoG [21] overexpression	ROS generator paraquat [23], toxins, produced by pathogenic bacteria [24,25]
interference with PQC	knockdown of Hspa9 [19], hsp-60 [17], dnj-21 [17], spg-7 [17]
interference with mitochondrial import and architecture	RNAi of tim-17, tim-23 (RNAi) [14,15], phb-2 [16,17]	arsenic (III) [14]
mtDNA depletion	RNAi of mtDNA helicase pif-1 [17], Deletor mice [34]	ethidium bromide [17,45]
interference with mitochondrial translation	downregulation of various cytosolic and mitochondrial ribosomal proteins [17,26]	bacterial and mitochondrial translation inhibitors doxycycline and chloramphenicol [26]
loss of ETC subunits	cco-1 RNAi [27], isp-1 (qm150) [44], clk-1 (qm30) [44] alleles, RNAi of ND75 [41], Surf1^−/− mice [42]	ETC inhibitors antimycin [23,24], rotenone [23]
sirtuin activation and mitochondrial biogenesis	sir-2.1 overexpression [29]	PARP inhibitors MRL45696 [30] and AZD2281 [29], NAD⁺ precursor NR [29], rapamycin [26]