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telomeres in green
Image by Claus Azzalin
Research published in The EMBO Journal suggests that p53 has tumor suppressor functions related to telomeres.
The study showed, for the first time, that p53 can suppress accumulated DNA damage at telomeres.
P53 is known to regulate the genome’s integrity. When DNA is damaged, p53 helps activate the transcription of genes that regulate the cell cycle and induce apoptosis.
However, prior studies have shown that p53 can bind at many locations across the genome, including sites that are not responsible for activating these regulatory genes.
Paul Lieberman, PhD, of The Wistar Institute in Philadelphia, Pennsylvania, and his colleagues decided to study these binding sites to see if p53 and telomeres might be more closely related than previous research suggested.
“We believed that p53 may be responsible for a more direct protective effect in telomeres,” Dr Lieberman said.
Using ChIP-sequencing, he and his colleagues identified p53 binding sites in subtelomeres.
They found that when p53 was bound to subtelomeres, the protein was able to suppress the formation of a histone modification called γ-H2AX.
This histone is modified in greater amounts when there is a double-strand break on DNA. If it persists, the break is not repaired, so suppressing its expression means the DNA is being preserved.
Additionally, p53 was able to prevent DNA degradation in telomeres, thereby keeping them intact and allowing them to more properly protect the tips of chromosomes.
“Based on our findings, we propose that the modifications to chromatin made by p53 enhance local DNA repair or protection,” Dr Lieberman said. “This would be yet another tumor suppressor function of p53, thus providing additional framework for just how important this gene is in protecting us from cancer.” 
telomeres in green
Image by Claus Azzalin
Research published in The EMBO Journal suggests that p53 has tumor suppressor functions related to telomeres.
The study showed, for the first time, that p53 can suppress accumulated DNA damage at telomeres.
P53 is known to regulate the genome’s integrity. When DNA is damaged, p53 helps activate the transcription of genes that regulate the cell cycle and induce apoptosis.
However, prior studies have shown that p53 can bind at many locations across the genome, including sites that are not responsible for activating these regulatory genes.
Paul Lieberman, PhD, of The Wistar Institute in Philadelphia, Pennsylvania, and his colleagues decided to study these binding sites to see if p53 and telomeres might be more closely related than previous research suggested.
“We believed that p53 may be responsible for a more direct protective effect in telomeres,” Dr Lieberman said.
Using ChIP-sequencing, he and his colleagues identified p53 binding sites in subtelomeres.
They found that when p53 was bound to subtelomeres, the protein was able to suppress the formation of a histone modification called γ-H2AX.
This histone is modified in greater amounts when there is a double-strand break on DNA. If it persists, the break is not repaired, so suppressing its expression means the DNA is being preserved.
Additionally, p53 was able to prevent DNA degradation in telomeres, thereby keeping them intact and allowing them to more properly protect the tips of chromosomes.
“Based on our findings, we propose that the modifications to chromatin made by p53 enhance local DNA repair or protection,” Dr Lieberman said. “This would be yet another tumor suppressor function of p53, thus providing additional framework for just how important this gene is in protecting us from cancer.”
telomeres in green
Image by Claus Azzalin
Research published in The EMBO Journal suggests that p53 has tumor suppressor functions related to telomeres.
The study showed, for the first time, that p53 can suppress accumulated DNA damage at telomeres.
P53 is known to regulate the genome’s integrity. When DNA is damaged, p53 helps activate the transcription of genes that regulate the cell cycle and induce apoptosis.
However, prior studies have shown that p53 can bind at many locations across the genome, including sites that are not responsible for activating these regulatory genes.
Paul Lieberman, PhD, of The Wistar Institute in Philadelphia, Pennsylvania, and his colleagues decided to study these binding sites to see if p53 and telomeres might be more closely related than previous research suggested.
“We believed that p53 may be responsible for a more direct protective effect in telomeres,” Dr Lieberman said.
Using ChIP-sequencing, he and his colleagues identified p53 binding sites in subtelomeres.
They found that when p53 was bound to subtelomeres, the protein was able to suppress the formation of a histone modification called γ-H2AX.
This histone is modified in greater amounts when there is a double-strand break on DNA. If it persists, the break is not repaired, so suppressing its expression means the DNA is being preserved.
Additionally, p53 was able to prevent DNA degradation in telomeres, thereby keeping them intact and allowing them to more properly protect the tips of chromosomes.
“Based on our findings, we propose that the modifications to chromatin made by p53 enhance local DNA repair or protection,” Dr Lieberman said. “This would be yet another tumor suppressor function of p53, thus providing additional framework for just how important this gene is in protecting us from cancer.”