Maintenance of Mitochondrial Morphology by Autophagy and Its Role in High Glucose Effects on Chronological Lifespan of Saccharomyces cerevisiae
Table 1
The percentage of wild-type and mutant cells showing completely fragmented mitochondrial morphology in cultures incubated in three different concentrations of glucose (0.5%, 2%, and 4%) at the times indicated.
Strain
0.5% glucose
2% glucose
4% glucose
24 h
48 h
72 h
24 h
48 h
72 h
24 h
48 h
72 h
Wild type
1.6 (0.7)
2.4 (0.9)
2.2 (1.2)
6.5 (0.8)
36.0 (1.1)
63.6 (4.3)
10.7 (2.1)
38.2 (7.5)
66.2 (6.7)
dnm1
0.8 (1.3)
0.8 (0.9)
2.9 (1.2)
1.3 (1.5)
22.4 (1.0)
45.1 (1.3)
3.6 (1.5)
29.5 (2.2)
67.5 (1.9)
fis1
n.d.
n.d.
n.d.
1.8 (1.1)
7.3 (2.1)
30.2 (1.5)
6.3 (0.8)
13.3 (1.2)
63.2 (5.7)
tor1
1.0 (1.0)
0.9 (0.3)
1.5 (0.7)
6.1 (0.3)
8.2 (1.1)
36.7 (0.9)
11.3 (1.2)
27.0 (1.0)
41.4 (1.0)
gpa2
1.7 (0.6)
1.2 (0.4)
4.9 (0.6)
6.3 (0.6)
39.7 (3.7)
67.7 (1.7)
5.6 (1.6)
34.7 (1.0)
54.8 (1.0)
snf3
1.9 (0.4)
3.8 (0.5)
6.0 (0.7)
5.5 (0.7)
32.9 (3.1)
47.7 (2.3)
8.5 (1.9)
71.2 (4.2)
75.4 (5.4)
rgt2
n.d.
n.d.
n.d.
5.3 (1.9)
28.8 (3.6)
50.7 (2.6)
8.3 (2.2)
22.7 (2.9)
72.4 (6.2)
pde1
0.8 (0.7)
1.0 (0.4)
1.3 (1.2)
11.9 (1.5)
60.0 (2.0)
78.4 (1.6)
16.3 (3.1)
61.7 (2.2)
70.5 (2.9)
pde2
4.8 (0.1)
3.8 (0.9)
9.3 (4.3)
6.8 (1.5)
56.1 (5.4)
84.6 (1.7)
16.6 (4.8)
48.0 (8.4)
68.1 (2.9)
uth1
3.1 (1.7)
2.9 (0.4)
6.8 (3.0)
7.5 (2.2)
37.0 (4.4)
54.9 (2.6)
14.0 (3.3)
34.0 (7.5)
63.0 (5.1)
atg32
n.d.
n.d.
n.d.
8.2 (1.7)
27.6 (2.8)
50.1 (4.2)
9.3 (1.5)
60.2 (1.6)
68.4 (4.3)
atg1
14.8 (5.2)
8.0 (0.7)
12.0 (1.7)
14.4 (1.4)
57.7 (1.0)
74.6 (0.8)
13.0 (2.2)
60.5 (7.2)
74.4 (0.5)
Wild type + rapamycin1
2.8 (0.2)
3.2 (0.3)
4.2 (0.7)
3.9 (0.6)
6.2 (1.3)
12.0 (0.9)
5.6 (1.5)
7.6 (1.0)
14.9 (0.9)
uth1 + rapamycin1
2.5 (0.6)
2.6 (0.8)
2.1 (0.4)
2.5 (0.7)
3.6 (0.5)
5.9 (0.7)
3.8 (0.9)
6.1 (0.5)
17.2 (1.6)
atg1 + rapamycin1
7.4 (0.5)
10.1 (1.5)
13.5 (1.6)
9.0 (0.4)
30.8 (1.4)
62.5 (0.9)
12.9 (0.8)
31.1 (1.8)
67.4 (0.7)
Wild-type cells or mutants were grown in the presence of 10 nM rapamycin.
*The fis1Δ strain used in these experiments has been shown to also carry a mutation in the WHI2 gene which rescues the mitochondrial respiratory defect caused by FIS1 deficiency, but which also causes a failure to suppress cell growth during amino acid deprivation [29].
