Then, they showed that when the cancer cells didn't make enough ATRX, the cells couldn't join together the two
ends of a broken DNA strand.
Not exact matches
James Christiansen, professor
of biology at Drake University in DesMoines, is studying how telomeres, the simple, non-genetic DNAsequences that sheathe the
ends of chromosomes, function in reptiles.Each time a healthy human cell divides, it loses a little bit
of thetelomere, until the strands are too short to protect the chromosomes.At that point the
DNA in a cell begins to
break down, which triggerssenescence and death.
Previous studies have implicated the
DNA polymerase θ (Polθ also known as POLQ, encoded by POLQ) in a pathway required for the repair
of DNA double - strand
breaks, referred to as the error - prone microhomology - mediated
end - joining (MMEJ) pathway.
For example, non-homologous
end - joining is involved in the development
of lymphocytes in resolving recombination intermediates i.e.,
DNA strand
breaks (DSBs) that occur during V (D) J recombination.
(2016) RB localizes to
DNA double - strand
breaks and promotes
DNA end resection and homologous recombination through the recruitment
of BRG1.
Zinc finger nucleases [1], [2], transcription activator - like effector nucleases [3], [4] and homing meganucleases [5] have provided powerful tools to induce targeted mutations in the form
of small insertions or deletions derived from
DNA break repair
of nonhomologous
end joining (NHEJ) or homologous recombination.
Cells lacking HRR must repair double - strand
DNA breaks through more error - prone forms
of DNA repair such as nonhomologous
end joining.
They protect chromosome
ends from being mistaken for
broken pieces
of DNA that would otherwise be fixed by cellular repair machinery.
This pre-lab activity would allow them to use different «chemical tools» to
break down the various parts
of the cell and, in the
end, identify a list
of materials needed to complete the
DNA extraction lab.