Nuclear-encoded mitochondrial complex I gene expression is restored to normal levels by inhibition of unedited ATP9 transgene expression in A. thaliana

MARÍA V. BUSI; DIEGO F. GÓMEZ-CASATI; MARIANO PERALES; ALEJANDRO ARAYA; EDUARDO ZABALETA

PLANT PHYSIOLOGY AND BIOCHEMISTRY

ELSEVIER

Año: 2006 vol. 44 p. 1 - 6

0981-9428

Mitochondria play an important role during sporogenesis in plants. The steady state levels of the nuclear-encoded mitochondrial complex I (nCI), PSST, TYKY and NADHBP transcripts increase in flowers of male-sterile plants with impairment of mitochondrial function generated by the expression of the unedited version of ATP9 (u-ATP9). This suggests a nuclear control of nCI genes in response to the mitochondrial flaw. To evaluate this hypothesis, transgenic plants carrying the GUS reporter gene, under the control of the PSST, TYKY and NADHBP promoters, were constructed. We present evidence that suppression by antisense strategy of the expression of u-ATP9 restores the normal levels of three nCI transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. constructed. We present evidence that suppression by antisense strategy of the expression of u-ATP9 restores the normal levels of three nCI transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. constructed. We present evidence that suppression by antisense strategy of the expression of u-ATP9 restores the normal levels of three nCI transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. constructed. We present evidence that suppression by antisense strategy of the expression of u-ATP9 restores the normal levels of three nCI transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. evaluate this hypothesis, transgenic plants carrying the GUS reporter gene, under the control of the PSST, TYKY and NADHBP promoters, were constructed. We present evidence that suppression by antisense strategy of the expression of u-ATP9 restores the normal levels of three nCI transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. constructed. We present evidence that suppression by antisense strategy of the expression of u-ATP9 restores the normal levels of three nCI transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. transcripts, indicating that the increase in PSST, TYKY and NADHBP in plants with a mitochondrial flaw occurs at the transcriptional level. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here support the hypothesis that a mitochondrial dysfunction triggers a retrograde signaling which induce some nuclearencoded mitochondrial genes. Moreover, these results demonstrate that this is a valuable experimental model for studying nucleus–mitochondria cross-talk events. cross-talk events. cross-talk events. cross-talk events. The data presented here