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Mitochondria and regulation of cellular lifespan

Arabidopsis contains three antipodals, which undergo programmed cell death (PCD) around the timepoint of fertilization. As mentioned above, in lis, clo and ato mutants, antipodals adopt a central cell fate, which implies that the developmental program that results in antipodal PCD is repressed. However, it was initially unclear, how PCD in antipodal cells is activated or bypassed. Our recent characterization of the syco-1 mutant points to an important role for the central cell during this process (Kagi et al., 2010). In syco-1 mutants the two polar nuclei of the central cell fail to fuse and antipodal PCD is suppressed. SYCO codes for a mitochondria-localized cysteinyl-tRNA synthetase and in-situ hybridization and promoter reporter studies detect SYCO in the central cell of the female gametophyte, but not in the antipodals. Expression of SYCO under the central cell promoter MEDEA complements the syco-1 defect, indicating that antipodal PCD is regulated by the central cell. Ultrastructural analysis revealed that SYCO is necessary for the integrity of central cell mitochondria, whereas antipodal mitochondria appeared to be normal. To address whether there is a causal relationship between mitochondrial dysfunction in the central cell and the extended antipodal lifespan, we have manipulated the electron transport chain (ETC) of wild-type central cells by targeted expression of a dominant mitochondrial ATP/ADP translocator. This approach results in a phenocopy of syco-1 mutants, indicating that antipodal PCD is regulated by an ETC-dependent mobile factor generated in the central cell. 

Figure 1 Model for the regulation of antipodal PCD.

SYCO dependent ETC function triggers PCD in adjacent antipodal cells in a non-cell autonomous manner (Kägi et al., 2010). 

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