 |
PDBsum entry 5uiy
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Transcription
|
PDB id
|
|
|
|
5uiy
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
PDB id:
|
|
|
|
| Name: |
|
Transcription
|
|
|
Title:
|
|
Structure of bromodomain from human baz1a
|
|
Structure:
|
|
Bromodomain adjacent to zinc finger domain protein 1a. Chain: a, b, c, d. Fragment: unp residues 1425-1538. Synonym: atp-dependent chromatin-remodeling protein,atp-utilizing chromatin assembly and remodeling factor 1,hacf1,chrac subunit acf1, williams syndrome transcription factor-related chromatin-remodeling factor 180,wcrf180,hwalp1. Engineered: yes
|
|
Source:
|
|
Homo sapiens. Human. Organism_taxid: 9606. Gene: baz1a, acf1, wcrf180, hspc317. Expressed in: escherichia coli. Expression_system_taxid: 562
|
|
Resolution:
|
|
|
1.69Å
|
R-factor:
|
0.198
|
R-free:
|
0.235
|
|
|
Authors:
|
|
M.Oppikofer,J.Sudhamsu
|
|
Key ref:
|
|
M.Oppikofer
et al.
(2017).
Non-canonical reader modules of BAZ1A promote recovery from DNA damage.
Nat Commun,
8,
862.
PubMed id:
|
|
|
Date:
|
|
|
16-Jan-17
|
Release date:
|
12-Jul-17
|
|
|
|
|
|
|
PROCHECK
|
|
|
|
|
|
Headers
|
|
|
|
References
|
|
|
|
|
|
|
|
Q9NRL2
(BAZ1A_HUMAN) -
Bromodomain adjacent to zinc finger domain protein 1A from Homo sapiens
|
|
|
|
Seq:
Struc:
|
|
|
|
1556 a.a.
107 a.a.
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
 |
|
|
|
|
|
|
| |
|
|
Nat Commun
8:862
(2017)
|
|
PubMed id:
|
|
|
|
|
|
| |
|
Non-canonical reader modules of BAZ1A promote recovery from DNA damage.
|
|
M.Oppikofer,
M.Sagolla,
B.Haley,
H.M.Zhang,
S.K.Kummerfeld,
J.Sudhamsu,
E.M.Flynn,
T.Bai,
J.Zhang,
C.Ciferri,
A.G.Cochran.
|
|
|
|
|
| |
ABSTRACT
|
|
|
|
| |
|
|
Members of the ISWI family of chromatin remodelers mobilize nucleosomes to
control DNA accessibility and, in some cases, are required for recovery from DNA
damage. However, it remains poorly understood how the non-catalytic ISWI
subunits BAZ1A and BAZ1B might contact chromatin to direct the ATPase SMARCA5.
Here, we find that the plant homeodomain of BAZ1A, but not that of BAZ1B, has
the unusual function of binding DNA. Furthermore, the BAZ1A bromodomain has a
non-canonical gatekeeper residue and binds relatively weakly to acetylated
histone peptides. Using CRISPR-Cas9-mediated genome editing we find that BAZ1A
and BAZ1B each recruit SMARCA5 to sites of damaged chromatin and promote
survival. Genetic engineering of structure-designed bromodomain and plant
homeodomain mutants reveals that reader modules of BAZ1A and BAZ1B, even when
non-standard, are critical for DNA damage recovery in part by regulating ISWI
factors loading at DNA lesions and supporting transcriptional programs required
for survival.ISWI chromatin remodelers regulate DNA accessibility and have been
implicated in DNA damage repair. Here, the authors uncover functions, in
response to DNA damage, for the bromodomain of the ISWI subunit BAZ1B and for
the non-canonical PHD and bromodomain modules of the paralog BAZ1A.
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
 |
 |
 |
|
Links
