Skip to main content
. 2005 Jul;16(7):3438–3453. doi: 10.1091/mbc.E04-10-0894

Figure 2.

Figure 2.

The atg17Δ mutant is partially defective in autophagy. (A) The atg17Δ mutant is not defective in the Cvt pathway. Wild-type (SEY6210), atg1Δ (WHY001), vac8Δ (YTS178), atg17Δ (CWY239), atg17Δ vac8Δ (CWY332), and atg17Δ atg20Δ (CWY333) strains were grown in SMD and shifted to SD-N for the indicated times to induce autophagy. atg17Δ cells were not defective for processing of prApe1 by the Cvt or autophagy pathways. The atg17Δ mutation in combination with vac8Δ, but not atg20Δ, was blocked in the autophagic delivery of prApe1. (B) Pho8Δ60, a marker for nonspecific autophagy, indicates an autophagy defect in the atg17Δ strain. The wild-type (TN124), atg1Δ (HAY572), atg20Δ (D3Y112), vac8Δ (CWY278), atg17Δ (CWY279), and atg17Δ vac8Δ (HCY43) strains were grown in YPD and shifted to SD-N for 4 h. Samples were collected and protein extracts assayed for ALP activity. The results represent the mean and SD of three experiments.