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Biology subjects

Koduri, V.

Publications and source records attributed to Koduri, V..

3 recordsLinked to original sources

Positive Selection Screen for Natural Product β-Catenin Inactivators

Many genetically validated targets in cancer, including the transcription factor {beta}-catenin ({beta}-cat), have historically been viewed as undruggable. Cell-based phenotypic screening of chemical compounds can reveal new biological and pharmacological principles. Natural products are powerful probes because of their superior structural diversity, drug-like properties, and biological activities as compared to unoptimized synthetic compounds. We screened 326,304 natural product mixtures (40,744 extracts and 285,560 fractions derived from them) using mammalian cells expressing an oncogenic version of {beta}-cat fused to a suicide protein. Multiple fractions degraded the {beta}-cat fusion protein or drove it into a compartment where both fusion partners were apparently inactive. The active natural product from one of the latter specifically activates novel, but not classical, protein kinase Cs (PKCs) and thereby relocates {beta}-cat to juxtamembrane vacuolar structures. These findings suggest a path for inactivating oncogenic {beta}-cat and underscore the power of screening natural product collections with robust phenotypic assays.

cancer biology↗

Microglia Mitochondria Drive Neuronal Maturation via Metabolic and Transcriptional Reprogramming

Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by impaired social interactions, repetitive behaviors, and disrupted neuronal circuit maturation. Emerging evidence implicates both microglial function and mitochondrial regulation as critical determinants of ASD pathogenesis. Here, we identified microglia and their mitochondria as active modulators of neuronal circuit development, highlighting their potential roles as mechanistic contributors and biomarkers in ASD progression. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=147 SRC="FIGDIR/small/651306v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@6794ddorg.highwire.dtl.DTLVardef@5e71cborg.highwire.dtl.DTLVardef@80f0acorg.highwire.dtl.DTLVardef@138c828_HPS_FORMAT_FIGEXP M_FIG C_FIG

developmental biology↗

A transcriptional biosensor reveals mechanisms of α-ketoglutarate signaling to chromatin

Alpha-ketoglutarate (KG) is required for chromatin demethylation but mechanisms controlling KG abundance in the nucleus are poorly defined. Therefore, we designed a biosensor system to monitor this metabolite pool in human cells using an KG-responsive cyanobacterial transcription factor, NtcA. We then coupled this system with a genetic screen to identify genes that regulate KG in the nucleus, defining an inter-organelle pathway in which sequential mitochondrial activities of the GPT2 transaminase and SLC25A11 transporter supply nuclear KG. Using a mouse model of GPT2 deficiency, a human inborn error of metabolism, we found that this pathway controls chromatin methylation in the developing brain. Our work provides a tool to assess KG signaling to chromatin and a framework for leveraging forward genetics to study nuclear metabolite pools.

synthetic biology↗