DNA Damage Response in Elephant Cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA419061 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6307200_1.fastq.gz | Fastqsanger.gz | |||
| SRR6307200_2.fastq.gz | Fastqsanger.gz | |||
| SRR6307201_1.fastq.gz | Fastqsanger.gz | |||
| SRR6307201_2.fastq.gz | Fastqsanger.gz | |||
| SRR6307202_1.fastq.gz | Fastqsanger.gz |
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Project description:The identity of most functional elements in the mammalian genome and the phenotypes they impact are unclear. Here, we perform a genome-wide comparative analysis of patterns of accelerated evolution in species with highly distinctive traits to discover candidate functional elements for clinically important phenotypes. We identify accelerated regions (ARs) in the elephant, hibernating bat, orca, dolphin, naked mole rat and thirteen-lined ground squirrel lineages in mammalian conserved regions, uncovering ~33,000 elements that bind hundreds of different regulatory proteins in humans and mice. ARs in the elephant, the largest land mammal, are uniquely enriched at elephant DNA damage response genes and changed conserved regulatory sites. The genomic hotspot for elephant ARs is the E3 ligase subunit of the Fanconi Anemia Complex, a master regulator of DNA repair. Additionally, ARs in the six species are associated with specific human clinical phenotypes that have apparent concordance with overt traits in each species.
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Project description:Heldt2018 - Proliferation-quiescence decision
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This model is described in the article:
A comprehensive model for
the proliferation-quiescence decision in response to endogenous
DNA damage in human cells.
Heldt FS, Barr AR, Cooper S, Bakal
C, Novák B.
Proc. Natl. Acad. Sci. U.S.A. 2018 Feb;
:
Abstract:
Human cells that suffer mild DNA damage can enter a
reversible state of growth arrest known as quiescence. This
decision to temporarily exit the cell cycle is essential to
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proliferation-quiescence decision in nontransformed human
cells. We show that two bistable switches, the restriction
point (RP) and the G1/S transition, mediate this decision by
integrating DNA damage and mitogen signals. In particular, our
data suggest that the cyclin-dependent kinase inhibitor p21
(Cip1/Waf1), which is expressed in response to DNA damage,
promotes quiescence by blocking positive feedback loops that
facilitate G1 progression downstream of serum stimulation.
Intriguingly, cells exploit bistability in the RP to convert
graded p21 and mitogen signals into an all-or-nothing
cell-cycle response. The same mechanism creates a window of
opportunity where G1 cells that have passed the RP can revert
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response altogether, insulating S phase from mild, endogenous
DNA damage. Thus, two bistable switches conspire in the early
cell cycle to provide both sensitivity and robustness to
external stimuli.
This model is hosted on
BioModels Database
and identified by:
MODEL1703030000.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
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