Eukaryote chromosome integrity and stability since the telomeric DNA repeats and associated proteins prevent chromosome end-to-end TWS119 fusions and exonuclease degradation. The length of telomeres is a critical determinant of a cell’s replicative life span and telomere shortening has been linked to cell senescence, disease and ageing. Telomeres shorten with each cell division due to the so called end-replication problem, resulting in loss of telomeric repeats. The loss of telomeric repeats is compensated for by synthesis of new repeats. The enzyme responsible for synthesis of new repeats is the telomerase holoenzyme, which is an RNA-dependent DNA polymerase complex. This enzyme synthesises new tandem telomeric repeats de novo at the 39 chromosome strand end. Telomerase-negative cells experience telomere shortening and lose on average between 30 and 200 bp of telomeric sequence per cell division, a loss which is ultimately lethal. Telomerase consists of several subunits. The core subunit consists of Telomerase Reverse Transcriptase together with its conserved RNA component, which acts as the template for the synthesis of telomeric repeats. Telomere structure is dependent on multiple telomereassociated proteins and these proteins together with telomeric DNA form the so-called telosome. TAPs are part of the telomerase-mediated telomere maintenance and regulation mechanisms, including telomere loop formation. The gene encoding TERT has been deleted or mutated in a number of organisms which led to cell senescence and eventual cell death. The genome of malaria parasites is arranged into 14 linear chromosomes which contain telomeres consisting of 7-bp telomeric repeat sequences. The average telomere length per species varies, ranging from 850 bp to 6700 bp in the human parasites P. falciparum and P. vivax, respectively. Plasmodium telomere length appears to be kept constant during the erythrocytic cycle The genomes of different Plasmodium parasites contain a single copy tert gene. For TERT of P. falciparum it has been demonstrated that it is capable of de novo synthesis of telomeric repeats both to the 39 telomeric overhang and to non-telomeric 39 ends, thus contributing not only to telomere maintenance but also to adding new telomeric sequences to broken chromosomes. Telomerase activity in P. falciparum is detectable both in late stage trophozoites and schizonts, stages where DNA replication occurs. The RNA component of telomerase has been identified in silico in several Plasmodium species based on structural comparisons of conserved domains in TR domains from other organisms. The telomerase RNA is detectable in all erythrocytic stages and the ookinete stage of P. falciparum according to the PlasmoDB expression data. In order to analyse the importance of telomere metabolism/ dynamics for asexual blood stage multiplication of Plasmodium parasites we have attempted to generate mutants that lack expression of TERT. We have used the rodent malaria parasite P. berghei because of the high efficiency of transfection and rapid selection of gene-deletion mutants, which might be essential when TERT-deficient parasites show a delayed death phenotype as has been shown for other organisms. We found that we can target the P. berghei tert gene for gene deletion. However, our results also indicate that TERT is an essential enzyme for survival of P. berghei blood stages since we were unable to clone and propagate TERT-deficient parasites. This study reports an analysis of telomeres and telomerase of the rodent malaria parasite P. berghei and the unsuccessful attempts to isolate gene-deletion mutants lacking the gene encoding telomerase reverse transcriptase.