Mitochondrial contribution to the anoxic Ca2+ signal in maize suspension-cultured cells

被引:109
作者
Subbaiah, CC [1 ]
Bush, DS
Sachs, MM
机构
[1] Univ Illinois, Dept Crop Sci, Urbana, IL 61801 USA
[2] Rutgers State Univ, Dept Biol Sci, Newark, NJ 07102 USA
[3] USDA ARS, Plant Physiol & Genet Res Unit, Urbana, IL 61801 USA
关键词
D O I
10.1104/pp.118.3.759
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Anoxia induces a rapid elevation of the cytosolic Ca2+ concentration ([Ca2+](cyt)) in maize (Zea mays L.) cells, which is caused by the release of the ion from intracellular stores. This anoxic Ca2+ release is important for gene activation and survival in O-2-deprived maize seedlings and cells. In this study we examined the contribution of mitochondrial Ca2+ to the anoxic [Ca2+](cyt) elevation in maize cells. Imaging of intramitochondrial Ca2+ levels showed that a majority of mitochondria released their Ca2+ in response to anoxia and took up Ca2+ upon reoxygenation. We also investigated whether the mitochondrial Ca2+ release contributed to the increase in [Ca2+](cyt) under anoxia. Analysis of the spatial association between anoxic [Ca2+](cyt) changes and the distribution of mitochondrial and other intracellular Ca2+ stores revealed that the largest [Ca2+](cyt) increases occurred close to mitochondria and away from the tonoplast. In addition, carbonylcyanide p-trifluoromethoxyphenyl hydrazone treatment depolarized mitochondria and caused a mild elevation of [Ca2+](cyt) under aerobic conditions but prevented a [Ca2+](cyt) increase in response to a subsequent anoxic poise. These results suggest that mitochondria play an important role in the anoxic elevation of [Ca2+](cyt) and participate in the signaling of O-2 deprivation.
引用
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页码:759 / 771
页数:13
相关论文
共 57 条
  • [1] RELEASE OF CA2+ FROM INDIVIDUAL PLANT VACUOLES BY BOTH INSP(3) AND CYCLIC ADP-RIBOSE
    ALLEN, GJ
    MUIR, SR
    SANDERS, D
    [J]. SCIENCE, 1995, 268 (5211) : 735 - 737
  • [2] GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION
    ANKARCRONA, M
    DYPBUKT, JM
    BONFOCO, E
    ZHIVOTOVSKY, B
    ORRENIUS, S
    LIPTON, SA
    NICOTERA, P
    [J]. NEURON, 1995, 15 (04) : 961 - 973
  • [3] Ultrastructural and biochemical characterization of autophagy in higher plant cells subjected to carbon deprivation: Control by the supply of mitochondria with respiratory substrates
    Aubert, S
    Gout, E
    Bligny, R
    MartyMazars, D
    Barrieu, F
    Alabouvette, J
    Marty, F
    Douce, R
    [J]. JOURNAL OF CELL BIOLOGY, 1996, 133 (06) : 1251 - 1263
  • [4] SUPPRESSION OF MITOCHONDRIAL RESPIRATORY-FUNCTION AFTER SHORT-TERM ANOXIA
    AW, TY
    ANDERSSON, BS
    JONES, DP
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1987, 252 (04): : C362 - C368
  • [5] Mitochondrial participation in the intracellular Ca2+ network
    Babcock, DF
    Herrington, J
    Goodwin, PC
    Park, YB
    Hille, B
    [J]. JOURNAL OF CELL BIOLOGY, 1997, 136 (04) : 833 - 844
  • [6] Subcellular analysis of Ca2+ homeostasis in primary cultures of skeletal muscle myotubes
    Brini, M
    DeGiorgi, F
    Murgia, M
    Marsault, R
    Massimino, ML
    Cantini, M
    Rizzuto, R
    Pozzan, T
    [J]. MOLECULAR BIOLOGY OF THE CELL, 1997, 8 (01) : 129 - 143
  • [7] BROSNAN JM, 1993, PLANT CELL, V5, P931, DOI 10.1105/tpc.5.8.931
  • [8] Budd SL, 1996, J NEUROCHEM, V67, P2282
  • [9] BURNIER M, 1994, AM J PHYSIOL, V35, pC1118
  • [10] Bush DS, 1996, PLANTA, V199, P89, DOI 10.1007/BF00196885