NBS1 plays a synergistic role with telomerase in the maintenance of telomeres in Arabidopsis thaliana

We used Arabidopsis thaliana to study the possible functions of the DNA repair subunit, NBS1, in telomere homeostasis using knockout nbs1 mutants. The results showed that although NBS1-deficient plants were viable, lacked any sign of developmental aberration and produced fertile seeds through many generations upon self-fertilisation, plants also missing the functional telomerase (double mutants), rapidly, within three generations, displayed severe developmental defects. Cytogenetic inspection of cycling somatic cells revealed a very early onset of massive genome instability. Molecular methods used for examining the length of telomeres in double homozygous mutants detected much faster telomere shortening than in plants deficient in telomerase gene alone.Our findings suggest that NBS1 acts in concert with telomerase and plays a profound role in plant telomere renewal.The ends of linear eukaryotic chromosomes are protected by specific chromatin structures called telomeres that are composed of tandemly repeated telomeric DNA and proteins. In vertebrates, six specific proteins associate with telomeres having affinity to either single-stranded or double-stranded telomeric DNA and they are collectively called shelterin [1]. These complex structures are essential for chromosome stability, as they differentiate chromosome ends from DNA double-strand breaks (DSBs) [2]. They protect chromosome termini from nucleolytic attack and undesirable recombination. Telomeres also counterbalance incomplete replication of terminal DNA by conventional DNA polymerase [3]; cells have evolved specific telomerase reverse transcriptase (TERT), which can synthesise telomeric repeats using its own RNA template thus ensuring proper telomere length. In general, eukaryotic telomeres are composed of tandem G/C rich repeats that end in a single strand 3' overhang which can fold back and invade the duplex repeats to form the so-called T-loop [4]. In the absence of telomerase, telomeres become non-funct