Synaptotagmin10-cre, a driver to disrupt clock genes in the SCN

Jana Husse, Xunlei Zhou, Anton Shostak, Henrik Oster, Gregor Eichele*

*Corresponding author for this work
21 Citations (Scopus)


Surgical lesion of the suprachiasmatic nuclei (SCN) profoundly affects the circadian timing system. A complication of SCN ablations is the concomitant scission of SCN afferents and efferents. Genetic disruption of the molecular clockwork in the SCN provides a complementary, less invasive experimental approach. The authors report the generation and functional analysis of a new Cre recombinase driver mouse that evokes homologous recombination with high efficiency in the SCN. They inserted the Cre recombinase cDNA into the Synaptotagmin10 (Syt10) locus, a gene strongly expressed in the SCN. Heterozygous Synaptotagmin10-Cre (Syt10Cre) mice have no obvious circadian locomotor phenotype, and homozygous animals show slightly reduced light-induced phase delays. Crosses of Syt10Cre mice with β-galactosidase reporter animals revealed strong Cre activity in the vast majority of SCN cells. Cre activity is not detected in nonneuronal tissues with the exception of the testis. The authors demonstrate that conditionally deleting the clock gene Bmal1 using the Syt10Cre driver renders animals arrhythmic.

Original languageEnglish
JournalJournal of Biological Rhythms
Issue number5
Pages (from-to)379-389
Number of pages11
Publication statusPublished - 01.10.2011


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