Browsing by Author "Clement, Mark"

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    Inferring gene regulatory networks from asynchronous microarray data with AIRnet
    (BMC, 2010-11-02) Oviatt, David; Clement, Mark; Snell, Quinn; Sundberg, Kenneth; Lai, Chun Wan J.; Allen, Jared; Roper, Randall J.; Biology, School of Science
    Background Modern approaches to treating genetic disorders, cancers and even epidemics rely on a detailed understanding of the underlying gene signaling network. Previous work has used time series microarray data to infer gene signaling networks given a large number of accurate time series samples. Microarray data available for many biological experiments is limited to a small number of arrays with little or no time series guarantees. When several samples are averaged to examine differences in mean value between a diseased and normal state, information from individual samples that could indicate a gene relationship can be lost. Results Asynchronous Inference of Regulatory Networks (AIRnet) provides gene signaling network inference using more practical assumptions about the microarray data. By learning correlation patterns for the changes in microarray values from all pairs of samples, accurate network reconstructions can be performed with data that is normally available in microarray experiments. Conclusions By focussing on the changes between microarray samples, instead of absolute values, increased information can be gleaned from expression data.
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    Non-trisomic Homeobox Gene Expression during Craniofacial Development in the Ts65Dn Mouse Model of Down Syndrome
    (Wiley, 2013) Billingsley, Cherie N.; Allen, Jared R.; Baumann, Douglas D.; Deitz, Samantha L.; Blazek, Joshua D.; Newbauer, Abby; Darrah, Andrew; Long, Brad C.; Young, Brandon; Clement, Mark; Doerge, R. W.; Roper, Randall J.; Biology, School of Science
    Trisomy 21 in humans causes cognitive impairment, craniofacial dysmorphology, and heart defects collectively referred to as Down syndrome. Yet, the pathophysiology of these phenotypes is not well understood. Craniofacial alterations may lead to complications in breathing, eating, and communication. Ts65Dn mice exhibit craniofacial alterations that model Down syndrome including a small mandible. We show that Ts65Dn embryos at 13.5 days gestation (E13.5) have a smaller mandibular precursor but a normal sized tongue as compared to euploid embryos, suggesting a relative instead of actual macroglossia originates during development. Neurological tissues were also altered in E13.5 trisomic embryos. Our array analysis found 155 differentially expressed non-trisomic genes in the trisomic E13.5 mandible, including 20 genes containing a homeobox DNA binding domain. Additionally, Sox9, important in skeletal formation and cell proliferation, was upregulated in Ts65Dn mandible precursors. Our results suggest trisomy causes altered expression of non-trisomic genes in development leading to structural changes associated with DS. Identification of genetic pathways disrupted by trisomy is an important step in proposing rational therapies at relevant time points to ameliorate craniofacial abnormalities in DS and other congenital disorders.