Excess peroxisomes are degraded by autophagic machinery in mammals

被引:182
作者
Iwata, J
Ezaki, J
Komatsu, M
Yokota, S
Ueno, T
Tanida, I
Chiba, T
Tanaka, K
Kominami, E
机构
[1] Juntendo Univ, Sch Med, Dept Biochem, Bunkyo Ku, Tokyo 1138421, Japan
[2] Tokyo Metropolitan Inst Med Sci, Dept Mol Oncol, Tokyo 1138613, Japan
[3] Univ Yamanashi, Interdisciplinary Grad Sch Med & Engn, Biol Lab, Tamaho, Yamanashi 40938, Japan
关键词
D O I
10.1074/jbc.M512283200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Peroxisomes are degraded by autophagic machinery termed "pexophagy" in yeast; however, whether this is essential for peroxisome degradation in mammals remains unknown. Here we have shown that Atg7, an essential gene for autophagy, plays a pivotal role in the degradation of excess peroxisomes in mammals. Following induction of peroxisomes by a 2-week treatment with phthalate esters in control and Atg7-deficient livers, peroxisomal degradation was monitored within 1 week after discontinuation of phthalate esters. Although most of the excess peroxisomes in the control liver were selectively degraded within 1 week, this rapid removal was exclusively impaired in the mutant liver. Furthermore, morphological analysis revealed that surplus peroxisomes, but not mutant hepatocytes, were surrounded by autophagosomes in the control. Our results indicated that the autophagic machinery is essential for the selective clearance of excess peroxisomes in mammals. This is the first direct evidence for the contribution of autophagic machinery in peroxisomal degradation in mammals.
引用
收藏
页码:4035 / 4041
页数:7
相关论文
共 38 条
  • [11] Autophagy, cytoplasm-to-vacuole targeting pathway, and pexophagy in yeast and mammalian cells
    Kim, J
    Klionsky, DJ
    [J]. ANNUAL REVIEW OF BIOCHEMISTRY, 2000, 69 : 303 - 342
  • [12] Cvt9/Gsa9 functions in sequestering selective cytosolic cargo destined for the vacuole
    Kim, J
    Kamada, Y
    Stromhaug, PE
    Guan, J
    Hefner-Gravink, A
    Baba, M
    Scott, SV
    Ohsumi, Y
    Dunn, WA
    Klionsky, DJ
    [J]. JOURNAL OF CELL BIOLOGY, 2001, 153 (02) : 381 - 396
  • [13] Uth1p is involved in the autophagic degradation of mitochondria
    Kissová, I
    Deffieu, M
    Manon, S
    Camougrand, N
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (37) : 39068 - 39074
  • [14] Vacuolar import of proteins and organelles from the cytoplasm
    Klionsky, DT
    Ohsumi, Y
    [J]. ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 1999, 15 : 1 - 32
  • [15] Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice
    Komatsu, M
    Waguri, S
    Ueno, T
    Iwata, J
    Murata, S
    Tanida, I
    Ezaki, J
    Mizushima, N
    Ohsumi, Y
    Uchiyama, Y
    Kominami, E
    Tanaka, K
    Chiba, T
    [J]. JOURNAL OF CELL BIOLOGY, 2005, 169 (03) : 425 - 434
  • [16] BIOGENESIS OF PEROXISOMES
    LAZAROW, PB
    FUJIKI, Y
    [J]. ANNUAL REVIEW OF CELL BIOLOGY, 1985, 1 : 489 - 530
  • [17] Perspective - Selective mitochondrial autophagy, or mitophagy, as a targeted defense against oxidative stress, mitochondrial dysfunction, and aging
    Lemasters, JJ
    [J]. REJUVENATION RESEARCH, 2005, 8 (01) : 3 - 5
  • [18] A protein conjugation system essential for autophagy
    Mizushima, N
    Noda, T
    Yoshimori, T
    Tanaka, Y
    Ishii, T
    George, MD
    Klionsky, DJ
    Ohsumi, M
    Ohsumi, Y
    [J]. NATURE, 1998, 395 (6700) : 395 - 398
  • [19] Autophagy defends cells against invading group a Streptococcus
    Nakagawa, I
    Amano, A
    Mizushima, N
    Yamamoto, A
    Yamaguchi, H
    Kamimoto, T
    Nara, J
    Funao, J
    Nakata, M
    Tsuda, K
    Hamada, S
    Yoshimori, T
    [J]. SCIENCE, 2004, 306 (5698) : 1037 - 1040
  • [20] NICHOLLSGRZEMSK.FA, 1992, BIOCHEM PHARMACOL, V7, P1395