% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Reichard:1048674,
author = {Reichard, Julia and Wolff, Philip and Xie, Song and Zuo, Ke
and Fullio, Camila L. and Du, Jian and Graff, Severin and
Linde, Jenice and Yildiz, Can Bora and Pitschelatow, Georg
and Nabbefeld, Gerion and Dorp, Lilli and Vollmer, Johanna
and Biemans, Linda and Kempf, Shirley and Singh, Minali and
Mohan, K. Naga and Kuo, Chao-Chung and Vogel, Tanja and
Carloni, Paolo and Musall, Simon and Zimmer-Bensch,
Geraldine},
title = {{DNMT}1-mediated regulation of somatostatin-positive
interneuron migration impacts cortical architecture and
function},
journal = {Nature Communications},
volume = {16},
number = {1},
issn = {2041-1723},
address = {[London]},
publisher = {Springer Nature},
reportid = {FZJ-2025-04797},
pages = {6834},
year = {2025},
abstract = {The coordinated development of cortical circuits composed
of excitatory and inhibitory neurons is critical for proper
brain function, and disruptions are linked to a spectrum of
neuropsychiatric disorders. While excitatory neurons are
generated locally in the cortical proliferative zones,
inhibitory cortical interneurons (cINs) originate in the
basal telencephalon and migrate tangentially into the
cortex. Here, we show that DNA methyltransferase 1 (DNMT1)
is essential for the migration and integration of
somatostatin (SST)-expressing interneurons in mice. Dnmt1
deletion causes premature exit of SST+ cINs from the
superficial migratory stream and alters the expression of
key developmental genes. Unexpectedly, Dnmt1-deficient SST+
interneurons also exert non-cell-autonomous effects on
cortical progenitor cells, resulting in subtle yet lasting
alterations in cortical layering. These findings propose a
role for DNMT1 in governing the migration of SST+
interneurons and mediating their instructive signaling to
cortical progenitor cells, thereby shaping cortical
architecture and influencing long-term network function.},
cin = {INM-9 / IBI-3},
ddc = {500},
cid = {I:(DE-Juel1)INM-9-20140121 / I:(DE-Juel1)IBI-3-20200312},
pnm = {5252 - Brain Dysfunction and Plasticity (POF4-525) / 5231 -
Neuroscientific Foundations (POF4-523)},
pid = {G:(DE-HGF)POF4-5252 / G:(DE-HGF)POF4-5231},
typ = {PUB:(DE-HGF)16},
doi = {10.1038/s41467-025-62114-0},
url = {https://juser.fz-juelich.de/record/1048674},
}