This inability to synthesize in the 3→5 directionality is compensated with the use of Okazaki fragments, short pieces of DNA that are synthesized 5→3 from the 3→5 as the replication fork moves. As DNA polymerase requires RNA primers for DNA binding in order to commence replication, each Okazaki fragment is thus preceded by an RNA primer on the strand being synthesized. When the end of the chromosome is reached, the final RNA primer is placed upon this nucleotide region, and it is inevitably removed. Unfortunately once the primer is removed, DNA polymerase is unable to synthesize the remaining bases.Sufferers of DKC have been shown to have a reduction in TERC levels invariably affecting the normal function of telomerase which maintains these telomeres. With TERC levels down, telomere maintenance during development suffers accordingly. In humans, telomerase is inactive in most cell types after early development (except in extreme cases such as cancer). Thus, if telomerase is not able to efficiently affect the DNA in the beginning of life, chromosomal instability becomes a grave possibility in individuals much earlier than would be expected. A study shows that proliferative defects in DC skin keratinocytes are corrected by expression of the telomerase reverse transcriptase, TERT, or by activation of endogenous telomerase through expression of papillomavirus E6/E7 of the telomerase RNA component, TERC. Diagnosis
Since the disease has a wide variety of symptoms due to involvement of multiple systems of the body, diagnostic testing depends on the clinical findings in each individual patient.
Therapeutically, methods aimed at increasing TERC expression could prove beneficial in DKC. See also
Cutaneous conditions
List of cutaneous conditions

References
External links
GeneReviews/NCBI/NIH/UW entry on Dyskeratosis Congenita
Dyskeratosis Congenita research study of Inherited Bone Marrow Failure Syndromes (IBMFS)