Techniques to Study Autophagy in Plants

Table 1

Phenotypes caused by ATG gene modifications in Arabidopsis thaliana. E64d, inhibitor of lysosomal/vacuolar hydrolases; Concanamycin A, inhibitor of vacuolar (V-type) ATPase, preventing lysosomal/vacuolar degradation:HR-PCD (hypersensitive response programmed cell death).

Genotype	Phenotype	Reference(s)
Atg2-deficient	No autophagic inclusions in root tips upon E64d treatment.	[52]
Atg4a-/ Atg4b-deficient	Upon nitrogen starvation, no autophagosome formation and no delivery of GFP-Atg8 to the vacuole.	[54]
Atg5-deficient	Inhibition of rubisco containing body formation.	[90]
	No autophagic vesicles in root tips after E64d treatment.	[52]
	No formation of Atg5/12 complex. Defective in autophagy induced by concanamycin A treatment.	[151]
	Senescence upon light and carbon or nitrogen limitation.	[55]
Atg6-deficient	Male sterility.	[152]
	HR-PCD sensitive. Early senescence.	[80]
	Developmental defects and impaired pollen germination.	[153]
Atg7-deficient	Hypersensitive to nutrient-limitation. Senescence.	[44]
Atg8-transgenic	Expression induced by starvation. Stress leads premature aging.	[57, 66]
Atg9-deficient	Under carbon and nitrogen starvation, accelerated chlorosis.	[53]
	Seed germination impaired and leaf senescence accelerated.
	Weak decrease of autophagic vesicle accumulation following E64d treatment.	[52]
Atg10-deficient	Hypersensitive to nitrogen and carbon starvation. Early senescence and PCD.	[89]
	No formation of Atg5/12 complex. Defective in autophagy induced by concanamycin A treatment.	[151]
Atg18a-transgenic	Hypersensitivity to sucrose and nitrogen starvation. Premature senescence.	[154]