• Something wrong with this record ?

NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development

R. Bohuslavova, V. Fabriciova, O. Smolik, L. Lebrón-Mora, P. Abaffy, S. Benesova, D. Zucha, L. Valihrach, Z. Berkova, F. Saudek, G. Pavlinkova

. 2023 ; 14 (1) : 5554. [pub] 20230909

Language English Country England, Great Britain

Document type Journal Article, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc23016256

NEUROD1 is a transcription factor that helps maintain a mature phenotype of pancreatic β cells. Disruption of Neurod1 during pancreatic development causes severe neonatal diabetes; however, the exact role of NEUROD1 in the differentiation programs of endocrine cells is unknown. Here, we report a crucial role of the NEUROD1 regulatory network in endocrine lineage commitment and differentiation. Mechanistically, transcriptome and chromatin landscape analyses demonstrate that Neurod1 inactivation triggers a downregulation of endocrine differentiation transcription factors and upregulation of non-endocrine genes within the Neurod1-deficient endocrine cell population, disturbing endocrine identity acquisition. Neurod1 deficiency altered the H3K27me3 histone modification pattern in promoter regions of differentially expressed genes, which resulted in gene regulatory network changes in the differentiation pathway of endocrine cells, compromising endocrine cell potential, differentiation, and functional properties.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc23016256
003      
CZ-PrNML
005      
20240624143637.0
007      
ta
008      
231013s2023 enk f 000 0|eng||
009      
AR
024    7_
$a 10.1038/s41467-023-41306-6 $2 doi
035    __
$a (PubMed)37689751
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a enk
100    1_
$a Bohuslavova, Romana $u Laboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia $1 https://orcid.org/0000000161104688
245    10
$a NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development / $c R. Bohuslavova, V. Fabriciova, O. Smolik, L. Lebrón-Mora, P. Abaffy, S. Benesova, D. Zucha, L. Valihrach, Z. Berkova, F. Saudek, G. Pavlinkova
520    9_
$a NEUROD1 is a transcription factor that helps maintain a mature phenotype of pancreatic β cells. Disruption of Neurod1 during pancreatic development causes severe neonatal diabetes; however, the exact role of NEUROD1 in the differentiation programs of endocrine cells is unknown. Here, we report a crucial role of the NEUROD1 regulatory network in endocrine lineage commitment and differentiation. Mechanistically, transcriptome and chromatin landscape analyses demonstrate that Neurod1 inactivation triggers a downregulation of endocrine differentiation transcription factors and upregulation of non-endocrine genes within the Neurod1-deficient endocrine cell population, disturbing endocrine identity acquisition. Neurod1 deficiency altered the H3K27me3 histone modification pattern in promoter regions of differentially expressed genes, which resulted in gene regulatory network changes in the differentiation pathway of endocrine cells, compromising endocrine cell potential, differentiation, and functional properties.
650    12
$a endokrinní buňky $7 D055098
650    _2
$a buněčná diferenciace $x genetika $7 D002454
650    _2
$a transkripční faktory $7 D014157
650    _2
$a aktivace transkripce $7 D015533
650    12
$a beta-buňky $7 D050417
655    _2
$a časopisecké články $7 D016428
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Fabriciova, Valeria $u Laboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia
700    1_
$a Smolik, Ondrej $u Laboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia $1 https://orcid.org/0000000312502684
700    1_
$a Lebrón-Mora, Laura $u Laboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia $1 https://orcid.org/0009000262501217
700    1_
$a Abaffy, Pavel $u Laboratory of Gene Expression, Institute of Biotechnology CAS, 25250, Vestec, Czechia $1 https://orcid.org/0000000275718880
700    1_
$a Benesova, Sarka $u Laboratory of Gene Expression, Institute of Biotechnology CAS, 25250, Vestec, Czechia $1 https://orcid.org/0000000339565968
700    1_
$a Zucha, Daniel $u Laboratory of Gene Expression, Institute of Biotechnology CAS, 25250, Vestec, Czechia $1 https://orcid.org/0000000224691315
700    1_
$a Valihrach, Lukas $u Laboratory of Gene Expression, Institute of Biotechnology CAS, 25250, Vestec, Czechia $1 https://orcid.org/0000000267044337
700    1_
$a Berkova, Zuzana $u Diabetes Centre, Experimental Medicine Centre, Institute for Clinical and Experimental Medicine, 14021, Prague, Czechia $1 https://orcid.org/0000000180539978 $7 xx0081890
700    1_
$a Saudek, Frantisek $u Diabetes Centre, Experimental Medicine Centre, Institute for Clinical and Experimental Medicine, 14021, Prague, Czechia
700    1_
$a Pavlínková, Gabriela, $u Laboratory of Molecular Pathogenetics, Institute of Biotechnology CAS, 25250, Vestec, Czechia. gpavlinkova@ibt.cas.cz $1 https://orcid.org/0000000256896577 $d 1966- $7 xx0319150
773    0_
$w MED00184850 $t Nature communications $x 2041-1723 $g Roč. 14, č. 1 (2023), s. 5554
856    41
$u https://pubmed.ncbi.nlm.nih.gov/37689751 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y - $z 0
990    __
$a 20231013 $b ABA008
991    __
$a 20240624143634 $b ABA008
999    __
$a ok $b bmc $g 2000022 $s 1202618
BAS    __
$a 3
BAS    __
$a PreBMC-MEDLINE
BMC    __
$a 2023 $b 14 $c 1 $d 5554 $e 20230909 $i 2041-1723 $m Nature communications $n Nat Commun $x MED00184850
LZP    __
$a Pubmed-20231013

Find record

Citation metrics

Archiving options