E
Elisabeth M. Busch-Nentwich
Researcher at Wellcome Trust Sanger Institute
Publications - 57
Citations - 1949
Elisabeth M. Busch-Nentwich is an academic researcher from Wellcome Trust Sanger Institute. The author has contributed to research in topics: Zebrafish & Gene. The author has an hindex of 17, co-authored 41 publications receiving 1448 citations. Previous affiliations of Elisabeth M. Busch-Nentwich include University of Cambridge.
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Journal ArticleDOI
A systematic genome-wide analysis of zebrafish protein-coding gene function
Ross Kettleborough,Elisabeth M. Busch-Nentwich,Steven A. Harvey,Christopher M. Dooley,Ewart de Bruijn,Freek van Eeden,Ian M Sealy,Richard White,Colin Herd,Isaac J. Nijman,Fruzsina Fényes,Selina Mehroke,Catherine M Scahill,Richard Gibbons,Neha Wali,Samantha Carruthers,Amanda Hall,Jennifer Yen,Edwin Cuppen,Derek L. Stemple +19 more
TL;DR: An active project that aims to identify and phenotype the disruptive mutations in every zebra fish protein-coding gene, using a well-annotated zebrafish reference genome sequence, high-throughput sequencing and efficient chemical mutagenesis.
Journal ArticleDOI
Placentation defects are highly prevalent in embryonic lethal mouse mutants.
Vicente Perez-Garcia,Vicente Perez-Garcia,Elena Fineberg,Elena Fineberg,Robert Wilson,Alexander Murray,Alexander Murray,Cecilia Icoresi Mazzeo,Catherine Tudor,Arnold R. Sienerth,Arnold R. Sienerth,Jacqueline K. White,Elizabeth Tuck,Edward Ryder,Diane Gleeson,Emma Siragher,Hannah Wardle-Jones,Nicole Staudt,Neha Wali,John E. Collins,Stefan H. Geyer,Elisabeth M. Busch-Nentwich,Elisabeth M. Busch-Nentwich,Antonella Galli,James C. Smith,Elizabeth J. Robertson,David J. Adams,Wolfgang Weninger,Timothy J. Mohun,Myriam Hemberger,Myriam Hemberger +30 more
TL;DR: The screening of embryonic lethal and sub-viable mouse knockout lines from the Deciphering the Mechanisms of Developmental Disorders program for placental phenotypes found that 68% of knockout lines that are lethal at or after mid-gestation exhibited placental dysmorphologies, which highlight the hugely under-appreciated importance of placental defects in contributing to abnormal embryo development and suggest key molecular nodes that govern placenta formation.
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A high-resolution mRNA expression time course of embryonic development in zebrafish
Richard White,John E. Collins,Ian M Sealy,Neha Wali,Christopher M. Dooley,Zsofia Digby,Derek L. Stemple,Daniel N. Murphy,Konstantinos Billis,Thibaut Hourlier,Anja Füllgrabe,Matthew P. Davis,Anton J. Enright,Elisabeth M. Busch-Nentwich,Elisabeth M. Busch-Nentwich +14 more
TL;DR: An mRNA expression time course of zebrafish development across 18 time points from 1 cell to 5 days post-fertilisation sampling individual and pools of embryos shows a class of over 100 previously uncharacterised zinc finger domain containing genes, located on the long arm of chromosome 4, is expressed in a sharp peak during zygotic genome activation.
Journal ArticleDOI
scRNA-Seq reveals distinct stem cell populations that drive hair cell regeneration after loss of Fgf and Notch signaling.
Mark E. Lush,Diaz Dc,Nina Koenecke,Sungmin Baek,Helena Boldt,Madeleine K St Peter,Tatiana Gaitan-Escudero,Andrés Romero-Carvajal,Andrés Romero-Carvajal,Elisabeth M. Busch-Nentwich,Elisabeth M. Busch-Nentwich,Anoja Perera,Kathryn E Hall,Allison Peak,Jeffrey S. Haug,Tatjana Piotrowski +15 more
TL;DR: This work demonstrates that Fgf and Notch signaling inhibit proliferation of support cells in parallel by inhibiting Wnt signaling, which is crucial for identifying factors to trigger hair cell production in mammals.
Journal ArticleDOI
mRNA processing in mutant zebrafish lines generated by chemical and CRISPR-mediated mutagenesis produces unexpected transcripts that escape nonsense-mediated decay.
Jennifer L. Anderson,Timothy Mulligan,Meng-Chieh Shen,Hui Wang,Catherine M Scahill,Frederick J. Tan,Shao J. Du,Elisabeth M. Busch-Nentwich,Elisabeth M. Busch-Nentwich,Steven A. Farber +9 more
TL;DR: In this paper, the authors analyzed mRNA processing in seven zebrafish lines with mutations expected to disrupt gene function, generated by CRISPR/Cas9 or ENU mutagenesis methods.