Search bioRxiv⌕ Search

Biology subjects

Schiffmann, C.

Publications and source records attributed to Schiffmann, C..

2 recordsLinked to original sources

Phenotyping in the era of genomics: MaTrics a digital character matrix to document mammalian phenotypic traits coded numerically

A new and uniquely structured matrix of mammalian phenotypes, MaTrics (Mammalian Traits for Comparative Genomics) is presented in a digital form. By focussing on mammalian species for which genome assemblies are available, MaTrics provides an interface between mammalogy and comparative genomics. MaTrics was developed as part of a project to link phenotypic differences between mammals to differences in their genomes using Forward Genomics. Apart from genomes this approach requires information on homologous phenotypes that are numerically encoded (presence-absence; multistate character coding*) in a matrix. MaTrics provides these data, links them to at least one reference (e.g., literature, photographs, histological sections, CT-scans, or museum specimens) and makes them available in a machine actionable NEXUS-format. By making the data computer readable, MatTrics opens a new way for digitizing collections. Currently, MaTrics covers 147 mammalian species and includes 207 characters referring to structure, morphology, physiology, ecology and ethology. Researching these traits revealed substantial knowledge gaps, highlighting the need for substantial phenotyping efforts in the genomic era. Using the trait information documented in MaTrics, previous Forward Genomics screens identified changes in genes that are associated with various phenotypes, ranging from fully-aquatic lifestyle to dietary specializations. These results motivate the continuous expansion of phenotype information, both by filling research gaps or by adding additional taxa and traits. MaTrics is digitally available online within the data repository Morph{middle dot}D{middle dot}Base (www.morphdbase.de).

zoology↗

Epigenetic gene-expression links heart failure to memory impairment

In current clinical practice care of diseased patients is often restricted to separated disciplines. However, such an organ-centered approach is not always suitable. For example, cognitive dysfunction is a severe burden in heart failure patients. Moreover, these patients have an increased risk for age-associated dementias. The underlying molecular mechanisms are presently unknown and thus corresponding therapeutic strategies to improve cognition in heart failure patients are missing. Using mice as model organisms we show that heart failure leads to specific changes in hippocampal gene-expression, a brain region intimately linked to cognition. These changes reflect increased cellular stress pathways which eventually lead to loss of neuronal euchromatin and reduced expression of a hippocampal gene cluster essential for cognition. Consequently, mice suffering from heart failure exhibit impaired memory function. These pathological changes are ameliorated via the administration of a drug that promotes neuronal euchromatin formation. Our study provides first insight to the molecular processes by which heart failure contributes to neuronal dysfunction and point to novel therapeutic avenues to treat cognitive defects in heart failure patients.

neuroscience↗