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Overexpression of the Drosophila ATR homologous checkpoint kinase Mei-41 induces a G2/M checkpoint in Drosophila imaginal tissue

In Drosophila melanogaster, the ATR homologue meiotic 41 (mei-41) is pivotal to DNA damage repair and cell cycle checkpoint signalling. Although various mei-41 mutant alleles have been analyzed in the past, no gain-of-function allele is yet available. To fill this gap, the authors generated transgenic flies, allowing temporal and tissue-specific induction of mei-41. The authors conclude that overexpression of the Drosophila ATR homologue mei-41 elicits an effectual DNA damage response irrespective of irradiation.

Aims and scope

For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics. Articles covering novel viral sequences or the use of new technology and software in genomic research are also welcomed.

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Hereditas launched with BioMed Central in 2015, transferring from its previous publisher Wiley. All back content is available in the archive.

Editors-in-Chief

Stefan Baumgartner, Lund University
Yongyong Shi, Shanghai Jiao Tong University

Society information

The Mendelian Society of Lund was founded in 1910 and except for a short break during 1912-1916 has been active ever since. In 1920, the Society started to publish Hereditas, a scientific journal in genetics. In the post-genomic era, the scope of Hereditas has evolved to include any research on genomic analysis.

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