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CBCB scientists Senthil Kumar and Sridhar Hannenhalli publish a paper in PLOS Computational Biology on the dynamical model of CRISPR-mediated prokaryote-phage coevolution
"Regulated CRISPR Modules Exploit a Dual Defense Strategy of Restriction and Abortive Infection in a Model of Prokaryote-Phage Coevolution” article: http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.10...
CBCB faculty Eytan Ruppin’s group publishes a paper in Nature Communications on Non-Alcoholic Fatty Liver Disease
CBCB faculty Eytan Ruppin’s group has published a paper titled “Genome-scale study reveals reduced metabolic adaptability in patients with non-alcoholic fatty liver disease” on February 3, 2016 in the journal Nature Communications.
For further information, please see: https://www.cs.umd.edu/article/2016/02/researchers-steno-center-eytan-ru...
“Genome-scale study reveals reduced metabolic adaptability in patients with non-alcoholic fatty liver disease” article: http://www.nature.com/ncomms/2016/160203/ncomms9994/full/ncomms9994.html
Jeremy Selengut on Thompson's highly cited researcher list
CBCB faculty Eytan Ruppin’s group co-authors a paper in Nature on the diversion of aspartate in ASS1-deficient tumours, a study led by Ayelet Erez from the Weizmann Institute
Keren Yizhak from Eytan Ruppin’s group co-authored a paper titled “Diversion of aspartate in ASS1-deficient tumours fosters de novo pyrimidine synthesis”, published in Nature on November 11, 2015.
Cancer cells hijack and remodel existing metabolic pathways for their benefit. Argininosuccinate synthase (ASS1) is a urea cycle enzyme that is essential in the conversion of nitrogen from ammonia and aspartate to urea. A decrease in nitrogen flux through ASS1 in the liver causes the urea cycle disorder, citrullinaemia. In contrast to the well-studied consequences of loss of ASS1 activity on ureagenesis, the purpose of its somatic silencing in multiple cancers is largely unknown.
In this study, the authors show that decreased activity of ASS1 in cancers supports proliferation by facilitating pyrimidine synthesis via CAD (carbamoyl-phosphate synthase 2, aspartate transcarbamylase, and dihydroorotase complex) activation. Decreasing CAD activity by blocking citrin, the mTOR signalling, or pyrimidine synthesis decreases proliferation and thus may serve as a therapeutic strategy in multiple cancers where ASS1is downregulated. Their results demonstrate that ASS1downregulation is a novel mechanism supporting cancerous proliferation, and that ASS1 downregulation provides a metabolic link between the urea cycle enzymes and pyrimidine synthesis.
“Diversion of aspartate in ASS1-deficient tumours fosters de novo pyrimidine synthesis” article: http://www.nature.com/nature/journal/vaop/ncurrent/pdf/nature15529.pdf
CBCB scientists Eytan Ruppin and Rotem Katzir publish a paper in the Proceedings of the National Academy of Sciences (PNAS) on the quantitative identification of cancer SDLs in a model-based mechanistic manner
CBCB faculty Eytan Ruppin and CBCB doctoral student Rotem Katzir, along with collaborators, published a paper titled “Synthetic dosage lethality in the human metabolic network is highly predictive of tumor growth and cancer patient survival” on September 29, 2015 in the journal Proceedings of the National Academy of Sciences (PNAS).
Synthetic dosage lethality (SDL) denotes a genetic interaction between two genes whereby the underexpression of gene A combined with the overexpression of gene B is lethal. SDLs offer a promising way to kill cancer cells by inhibiting the activity of SDL partners of activated oncogenes in tumors, which are often difficult to target directly.
In this paper, a network-level computational modeling framework is introduced that quantitatively predicts human SDLs in metabolism. The approach presented can be used to identify SDLs in species and cell types in which “omics” data necessary for data-driven identification are missing. As expected, the predicted SDLs are less frequently active in tumors to avoid lethality. Cancer tumors with more and stronger SDLs have smaller tumor size and lead to increased patient survival. Beyond facilitating the development of novel anticancer therapies, model-based identification of metabolic SDLs can be used to model pathogenic bacteria and provide leads to new antibiotic targets.
“Synthetic dosage lethality in the human metabolic network is highly predictive of tumor growth and cancer patient survival” article: http://www.pnas.org/content/112/39/12217.full
CBCB scientists Matthew Oberhardt and Eytan Ruppin publish a paper in Nature Communications on predicting new organism-media pairings
Lead author and CBCB postdoctoral associate Matthew Oberhardt and CBCB faculty Eytan Ruppin, along with collaborators, have published a paper titled “Harnessing the landscape of microbial culture media to predict new organism-media pairings” on October 13, 2015 in the journal Nature Communications.
Culturing microorganisms is a critical step in understanding and utilizing microbial life. In this paper, Dr. Oberhardt, Dr. Ruppin, and collaborators map the landscape of existing culture media by extracting natural-language media recipes into a Known Media Database (KOMODO).
They leverage KOMODO to predict new organism–media pairings using a transitivity property (74% growth in new in vitro experiments) and a phylogeny-based collaborative filtering tool (83% growth in new in vitro experiments and stronger growth on predicted well-scored versus poorly scored media). These resources are integrated into a web-based platform that predicts media given an organism’s 16S rDNA sequence, facilitating future cultivation efforts.
“Harnessing the landscape of microbial culture media to predict new organism–media pairings” article: http://www.nature.com/ncomms/2015/151013/ncomms9493/full/ncomms9493.html
CBCB scientists Michael Cummings, Adam Bazinet, and Jessica Goodheart publish a paper in Royal Society Open Science that provides a well-supported phylogenetic hypothesis for Cladobranchia
Cladobranchia (Gastropoda: Nudibranchia) is a diverse (approx. 1000 species) but understudied group of sea slug molluscs. In order to fully comprehend the diversity of nudibranchs and the evolution of character traits within Cladobranchia, a solid understanding of evolutionary relationships is necessary.
CBCB faculty Michael Cummings, CBCB postdoctoral associate Adam Bazinet, and lead author and CBCB doctoral student Jessica Goodheart published a cover paper titled “Relationships within Cladobranchia (Gastropoda: Nudibranchia) based on RNA-Seq data: an initial investigation” on Sept. 23, 2015 in the journal Royal Society Open Science.
In this paper, they address some of the long-standing issues regarding the evolutionary history of Cladobranchia using RNA-Seq data (transcriptomes). Their data provides a well-supported and almost fully resolved phylogenetic hypothesis for Cladobranchia. Their results support the monophyly of Cladobranchia and the sub-clade Aeolidida, but reject the monophyly of Dendronotida.
“Relationships within Cladobranchia (Gastropoda: Nudibranchia) based on RNA-Seq data: an initial investigation” article: http://rsos.royalsocietypublishing.org/content/2/9/150196
A video on the mission and scope of CBCB is now posted to the UMIACS YouTube page
CBCB scientists Sridhar Hannenhalli and Avinash Das Sahu publish a paper in Nature Communications on a new method that identifies genetic factors that could contribute to the risk for heart disease
For the news release regarding this paper, please see: https://cmns.umd.edu/news-events/features/3282
“Bayesian integration of genetics and epigenetics detects putatively causal SNPs underlying expression variability” article: http://www.nature.com/ncomms/2015/151005/ncomms9555/full/ncomms9555.html
"UMD researchers develop method to identify genetic factors of heart diseases" article: http://www.diamondbackonline.com/news/umd-researchers-develop-method-to-...
CBCB faculty work with freshmen on the terrapin genome project as part of the FIRE program
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