It was even more surprising that for a large number of mitochondrial genes, polyadenylated transcripts became more abundant after moderate heat treatment. During evolution, mitochondrial genes have been integrated into nuclear genomes, where they may have developed into functional nuclear represents the 367 kb mitochondrial genome with complete copies of the mitochondrial regions A, B, C and D, and an additional internal part that contains two copies of a complete D region and two copies of a 41 kb section of the A region. Comparison of a 262 kb insert of the Arabidopsis nuclear mitochondrial DNA with the mitochondrial DNA region, revealed a 99.91% identity of the two genomes, and suggested that the mitochondrial DNA transfer into the nucleus occurred about 88,000 years ago. It is highly unlikely that the genes located on the numtDNA have undergone sufficient 2,6-Diaminopurine adaptation that would allow them to be expressed under the control of the nuclear compartment. Such adaptation would require the development of promoter sequences that allowed transcription by nuclear polymerases, and the establishment of 39signals that could be recognised by nuclear polyadenylation functions. It was therefore concluded that very little, if any, transcription occurs from numt genes. Our analysis of a model transcript, Mito1, which was selected because it allowed us to differentiate between transcripts derived from the mtDNA and the numtDNA, confirms the assumption that the numt gene is not transcribed. The four lines of evidence that point towards a mitochondrial origin of the polyadenylated Mito1 transcripts are its sequence identity with the mitochondrial gene, the failure to amplify nuclear transcripts, the lack of a CAP structure and the presence of multiple polyadenylation sites, a feature characteristic for mitochondrial transcripts. Enhanced polyA transcript UNC2881 levels quickly revert back to normal levels when the temperature is reduced to 24uC, which suggests that the heat treatment does not cause lasting damage.y contrast, components of the AP-1, AP-2 and AP-3 adaptor complexes did not colocalise with the spindle apparatus. Past controversy on changes in the endocytic rates during cell cycle progression suggests that it will prove important to explore the role of clathrin at the spindle in multiple cell-lines using multiple approaches.