Mitochondria, the powerhouses of our cells, are essential to life. Normal mitochondrial function is achieved through the cooperative interaction of the nuclear and mitochondrial genomes. New IVF approaches intended to circumvent devastating mitochondrial disease look set to change the ancient pattern of mtDNA inheritance and interaction with unknown consequences.

Plastids and mitochondria arose through endosymbiotic acquisition of formerly free-living bacteria. During more than a billion years of subsequent concerted evolution, the three genomes of plant cells have undergone dramatic structural changes to optimize the expression of the compartmentalized genetic material and to fine-tune the communication between the nucleus and the organelles. The chimeric composition of many multiprotein complexes in plastids and mitochondria (one part of the subunits being nuclear encoded and another one being encoded in the organellar genome) provides (...) a paradigm for co-evolution at the cellular level. In this paper, we discuss the co-evolution of nuclear and organellar genomes in the context of environmental adaptation in species and populations. We highlight emerging genetic model systems and new experimental approaches that are particularly suitable to elucidate the molecular basis of co-adaptation processes and describe how nuclear-cytoplasmic co-evolution can cause genetic incompatibilities that contribute to the establishment of hybridization barriers, ultimately leading to the formation of new species. (shrink)

Alternative pre‐mRNA splicing leads to distinct products of gene expression in development and disease. Antagonistic splice variants of genes involved in differentiation, apoptosis, invasion and metastasis often exist in a delicate equilibrium that is found to be perturbed in tumours. In several recent examples, splice variants that are overexpressed in cancer are expressed as hyper‐oncogenic proteins, which often correlate with poor prognosis, thus suggesting improved diagnosis and follow up treatment. Global gene expression technologies are just beginning to decipher the interplay (...) between alternatively spliced isoforms and protein‐splicing factors that will lead to identification of the mutations in these trans‐acting factors responsible for pathogenic alternative splicing in cancer. BioEssays 28: 378–386, 2006. © 2006 Wiley Periodicals, Inc. (shrink)