True about telomeres:
(A) Made up of repeated sequence of TTAGGG
(B) Telomerase shortens it
(C) it is shortened in cancer cells,
(D) It is responsible for cell ageing
"At birth, human telomeres are 15- to 20-kb pairs long and are composed of tandem repeats of a sixnucleotide
sequence (TTAGGG) that associates with specialized telomere-binding proteins to form a Tloop
structure that protects the ends of chromosomes from being mistakenly recognized as damaged. The
loss of telomeric repeats with each cell division cycle causes gradual telomere shortening, leading to
growth arrest (called senescence) when one or more critically short telomeres trigger a p53-regulated
DNA-damage checkpoint response"- 

How dividing cells can count their divisions is under intensive investigation. One likely mechanism is
that with each cell division, there is incomplete replication of chromosome ends (telomere shortening),
which ultimately results in cell cycle arrest. Telomeres are short repeated sequences of DNA (TTAGGG) present at the linear ends of chromosomes that are important for ensuring the complete replication of chromosome ends and protecting chromosomal termini from fusion and degradation.
When soma tic cells replicate, a small section ofthe telomere is not duplicated, and telomeres become progressively shortened.
As the telomeres become shorter, the ends of chromosomes cannot be protected and are seen as broken DNA, which signals cell cycle arrest. The lengths of the telomeres are normally maintained by nucleotide addition mediated by an enzyme called telomerase. 
Telomerase is a specialized RNA-protein complex that uses its own RNA as a template for adding nucleotides to the ends of
chromosomes The activity of telomerase is repressed by regulatory proteins, which restrict telomere elongation, thus providing a length sensing mechanism. Telomerase activity is expressed in germ cells and is present at low levels in stem cells, but it is usually absent in most somatic tissues. Therefore, as cells age, their telomeres become shorter, and they exit the cell cycle, resulting in an inability to generate new cells to replace damaged ones. Conversely, in immortal cancer cells, telomerase is reactivated, and telomeres are not shortened, 
suggesting that telomere elongation might be an important—possibly essential—step in tumor formation.
Despite such alluring observations, however, the relationship of telomerase activity and telomeric length
to aging and cancer still needs to be fully established
Germ cells and stem cells both contain active telomerase, but only the germ cells have sufficient levels of the enzyme to stabilize telomere length completely. Telomerase activation in cancer cells inactivates
the teleomericclock that limits the proliferative capacity of normal somatic cells.
AD
AB
BC
CA