High impact information on TEN1

• Here, we show that co-overexpressing TEN1 with a truncated form of STN1 efficiently bypasses the essential role of CDC13 [1].
• Thus, Stn1p and Ten1p control a Cdc13p-independent telomere capping mechanism that is coupled to the conventional DNA replication machinery [1].
• Other, temperature-sensitive, mutants of TEN1 arrested at G(2)/M via activation of the Rad9-dependent DNA damage checkpoint [2].
• We propose that Ten1 is required to regulate telomere length, as well as to prevent lethal damage to telomeric DNA [2].
• These ten1 mutant cells were found to accumulate single-stranded DNA in telomeric regions of the chromosomes [2].

Biological context of TEN1

• Increased dosage of STN1, especially in combination with increased dosage of TEN1, resulted in reduced telomere length that was indistinguishable from that in upf mutants [3].
• Chromosome end protection plasticity revealed by Stn1p and Ten1p bypass of Cdc13p [1].
• A binding defect between Stn1-13 and Ten1 was responsible for the long telomere phenotype of stn1-13 mutant cells [2].
• Increasing the levels of Stn1p and Ten1p in Upf+ cells is sufficient to delay senescence [4].

Other interactions of TEN1

• Moreover, rescue of the cdc13-1 mutation by STN1 was much improved when TEN1 was simultaneously overexpressed [2].

References