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Biology subjects

Rodrick, T.

Publications and source records attributed to Rodrick, T..

3 recordsLinked to original sources

A shotgun approach for highly multiplexed mammalian metabolic engineering

Mammalian metabolic engineering is critical to advancing basic biology, bioproduction, and cell therapy. However, as pathway complexity increases, so does the size of both the combinatorial design space and the DNA constructs required, rendering unbiased screens intractable. To address this, we developed Shotgun Genetic Engineering (SGE), a scalable approach that exploits the ease of delivering many barcoded small constructs--rather than a single large one--into mammalian cells. This allows each cell to serve as an independent experiment, carrying a unique synthetic metabolic pathway that explores combinations of gene content, stoichiometry, and organellar localization. Functional pathways are identified by sequencing barcodes from cells exhibiting the desired phenotype. Using SGE, we screened millions of pathway combinations to engineer essential amino acid biosynthesis in two mammalian cell lines (CHO and Jurkat), achieving near-wild-type growth in valine-free medium and, for the first time, enabling isoleucine prototrophy in CHO cells. Successful solutions favored mitochondrial localization and required integration of 23-52 kb of synthetic DNA--lengths that are impractical to screen by conventional methods. The resulting datasets are compatible with machine learning frameworks, positioning SGE as a powerful platform for decoding and engineering complex biosynthetic traits in mammalian systems.

synthetic biology↗

The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability

Glioblastoma (GBM) is the most common and aggressive primary brain malignancy. Adhesion G protein-coupled receptors (aGPCRs) have attracted interest for their functional role in gliomagenesis and their potential as treatment targets. To identify therapeutically targetable opportunities among aGPCR family members in unbiased fashion, we analyzed expression levels of all aGPCRs in GBM and non-neoplastic brain tissue. Using bulk and single cell transcriptomic and proteomic data, we show that CD97 (ADGRE5), an aGPCR previously implicated in GBM pathogenesis, is the most promising aGPCR target in GBM, by virtue of its abundance in all GBM tumors and its de novo expression profile in GBM compared to normal brain tissue and neural progenitors. CD97 knockdown or knockout significantly reduces the tumor initiation capacity of patient-derived GBM cultures (PDGC) in vitro and in vivo. Transcriptomic and metabolomic data from PDGCs suggest that CD97 promotes glycolytic metabolism. The oncogenic and metabolic effects of CD97 are mediated by the MAPK pathway. Activation of MAPK signaling depends on phosphorylation of the cytosolic C-terminus of CD97 and recruitment of {beta}-arrestin. Using single-cell RNA-sequencing and biochemical assays, we demonstrate that THY1/CD90 is the most likely CD97 ligand in GBM. Lastly, we show that targeting of PDGCs with an anti-CD97 antibody-drug conjugate in vitro selectively kills tumor cells but not human astrocytes or neural stem cells. Our studies identify CD97 as an important regulator of tumor metabolism in GBM, elucidate mechanisms of receptor activation and signaling, and provide strong scientific rationale for developing biologics to target it for therapeutic purposes.

cancer biology↗

Genome-wide analysis of dendritic cell differentiation

Dendritic cells (DCs) are immune sentinel cells that comprise antigen-presenting conventional DCs (cDCs) and cytokine-producing plasmacytoid DCs (pDCs). Cytokine Flt3 ligand (Flt3L) supports the proliferation of hematopoietic progenitors, and is also necessary and sufficient for DC differentiation. Here we characterized the spontaneous differentiation of a Flt3L-dependent murine progenitor cell line into pDCs and "myeloid" cDCs (cDC2s), and interrogated it using a genome-wide CRISPR/Cas9 dropout screen. The screen revealed multiple regulators of DC differentiation including the glycosylphosphatidylinositol transamidase complex, the Nieman-Pick type C cholesterol transporter and arginine methyltransferase Carm1; the role of Carm1 in pDC and cDC2 differentiation was confirmed by conditional targeting in vivo. We also found that negative regulators of mTOR signaling, including the subunits of TSC and GATOR1 complexes, restricted progenitor growth but enabled DC differentiation. The results provide a comprehensive forward genetic analysis of DC differentiation, and help explain how the opposing processes of proliferation and differentiation could be driven by the same cytokine.

immunology↗