About

Neal Bennett is an Assistant Professor of Professional Practice in Journalism and Media Studies at the School of Communication and Information at Rutgers University. His teaching focuses on a combination of media theory, workflows, and production, blending critical analysis with practical skills to equip students with a strong foundation in media principles, industry workflows, and creative storytelling. Bennett emphasizes both structure and experimentation in his instruction, helping students build technical proficiency, manage complex projects, and adapt to the evolving demands of media production. His approach has successfully prepared students for careers across the media industry, with many alumni working on major films, television shows, and diverse media projects. He is a multi-award-winning media professional and educator, having received multiple teaching awards from Rutgers University, including the 2023 Outstanding Faculty Honor Award. Bennett has earned Telly Awards and two Emmy recognitions for his work. He is actively involved in developing student media initiatives, leading the creation of a student video team at the School of Communication and Information and for The Daily Targum, as well as establishing a podcasting and video-production studio to support student media at Rutgers. In collaboration with the New Jersey Civic Information Consortium, he designs and implements media courses aimed at strengthening the pipeline from high school to college journalism and supporting local programming and community media initiatives.

Research topics

• Cell biology
• Biology
• Biochemistry
• Neuroscience
• Biotechnology
• Chemistry
• Endocrinology
• Genetics

Selected publications

• Genome-wide CRISPRi screen identifies basigin loss as protective in cardiac hypoxia

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-27

  article

  Cardiac function depends on continuous oxidative metabolism, rendering cardiomyocytes highly vulnerable to oxygen deprivation. Here, we performed a genome-wide CRISPR interference (CRISPRi) screen in human iPSC-derived cardiomyocytes to identify genes that modulate survival during chronic hypoxia. This screen revealed that knockdown of basigin (BSG), a chaperone for the monocarboxylate transporters MCT1 and MCT4, confers robust protection. Canonically, hypoxic cells suppress pyruvate dehydrogenase (PDH) activity to reduce the oxidation of major fuel sources, thereby limiting TCA cycle flux, lowering oxygen consumption, and minimizing reactive oxygen species generated by an overly reduced electron transport chain (ETC). In contrast, we found that BSG inhibition reverses this response, prioritizing ATP maintenance during hypoxia and enhancing cardiomyocyte survival. Mechanistically, BSG loss restricts lactate efflux, leading to decreased PDH phosphorylation and increased glucose uptake for oxidation. Consistent with this, ETC subunits are more essential under hypoxia, highlighting cardiomyocytes' unusual reliance on aerobic ATP production even when oxygen is limited. These findings challenge prevailing models of hypoxic adaptation by revealing cardiomyocyte-specific bioenergetic requirements and motivating future therapeutic efforts.

  PublisherDOI

• Genetic regulators of neuronal survival across metabolic environments

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-19

  articleOpen access1st author

  ABSTRACT Cellular energy metabolism and oxygen availability shape neuronal function and vulnerability, yet the genetic regulators of these metabolic processes in human neurons remain incompletely understood. Here, we performed CRISPR interference (CRISPRi) screens in human induced pluripotent stem cell (iPSC)-derived neurons across four distinct metabolic conditions and at three physiologically relevant oxygen tensions. This combinatorial approach enabled systematic interrogation of gene-environment interactions that govern neuronal metabolic adaptation. We identified genes—including genes associated with Leigh syndrome and autism spectrum disorder—whose importance for cell survival is highly sensitive to environmental context, revealing potential mechanisms underlying metabolic specification and selective neuronal vulnerability in neurological disorders. Our screens also uncovered regulators of neuronal glycolysis, including KIAA1429 and MAPT among others, which are previously uncharacterized modulators of neuronal glucose utilization and metabolic flexibility. Our work nominates candidate metabolic interventions and gene targets for enhancing neuronal resilience under hypoxic or nutrient-limited conditions.

  PublisherDOI

• Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production

  Proceedings of the National Academy of Sciences · 2024-01-11 · 21 citations

  articleOpen access1st author

  Respiratory chain dysfunction can decrease ATP and increase reactive oxygen species (ROS) levels. Despite the importance of these metabolic parameters to a wide range of cellular functions and disease, we lack an integrated understanding of how they are differentially regulated. To address this question, we adapted a CRISPRi- and FACS-based platform to compare the effects of respiratory gene knockdown on ROS to their effects on ATP. Focusing on genes whose knockdown is known to decrease mitochondria-derived ATP, we showed that knockdown of genes in specific respiratory chain complexes (I, III, and CoQ10 biosynthesis) increased ROS, whereas knockdown of other low ATP hits either had no impact (mitochondrial ribosomal proteins) or actually decreased ROS (complex IV). Moreover, although shifting metabolic conditions profoundly altered mitochondria-derived ATP levels, it had little impact on mitochondrial or cytosolic ROS. In addition, knockdown of a subset of complex I subunits—including NDUFA8 , NDUFB4 , and NDUFS 8—decreased complex I activity, mitochondria-derived ATP, and supercomplex level, but knockdown of these genes had differential effects on ROS. Conversely, we found an essential role for ether lipids in the dynamic regulation of mitochondrial ROS levels independent of ATP. Thus, our results identify specific metabolic regulators of cellular ATP and ROS balance that may help dissect the roles of these processes in disease and identify therapeutic strategies to independently target energy failure and oxidative stress.

  PublisherOA PDFDOI

• Abstract 4653: Unraveling the vulnerabilities of targeted therapy-tolerant persister cells in NSCLC

  Cancer Research · 2024-03-22

  article

  Abstract Genetic profiling and the development of targeted therapy has improved survival of many cancer patients, but resistance to targeted therapy remains a major barrier to long-term patient survival. To develop more pro-active strategies to improve clinical outcomes, our research focuses on drug-tolerant persister cells that constitute a reservoir of cancer cells that survive and adapt during the initial stage of therapy. These cells typically display therapy resistance in a reversible manner and set the stage for the subsequent emergence of cells with full acquired resistance. We utilized quantitative proteomics to characterize persister cells generated from EGFRmut, KRASmut, and ALKmut non-small cell lung cancer (NSCLC) cell lines after treatment with osimertinib, sotorasib, and lorlatinib, respectively. Integrating proteomics data with network analysis revealed a decrease in the signaling network associated with cell cycle regulation and DNA replication. Meanwhile, persister cells exhibited an enrichment in proteins linked to lysosomes, amino acids, and fatty acid metabolism. The data revealed a consistent metabolic shift in persister cells, with an increased dependence on oxidative phosphorylation (OXPHOS) for ATP generation. Small-scale drug screening was performed based on findings from proteomics and confirmed that persister cells are vulnerable to inhibitors of OXPHOS mitochondrial complexes. Combination treatment of OXPHOS inhibitors and each targeted therapy delayed the emergence of resistance. One complex V inhibitor, Gboxin, selectively inhibited the growth of persister cells. The therapeutic potential of complex V was further validated by CRISPR-based genetic knockdown studies. The metabolic transition in drug tolerant persister cells may serve as a critical adaptive resistance mechanism to provide a survival advantage under targeted therapy-induced stress. Understanding this metabolic shift may lead to new treatments that aim to prevent or delay the onset of acquired resistance in NSCLC. Citation Format: Donghwa Kim, Dmitry Kuchenov, Aubhishek Zaman, Neal Bennett, Emilio Ramos, Ken Nakamura, Arun P. Wiita, Sourav Bandyopadhyay, Trever Bivona. Unraveling the vulnerabilities of targeted therapy-tolerant persister cells in NSCLC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4653.

  PublisherDOI

• Abstract 5424: Respiratory function linked to <i>in vivo</i> metastatic lung cancer progression

  Cancer Research · 2024-03-22

  article

  Abstract Metastases are a major cause of morbidity and mortality in patients with cancer. How metastatic tumors employ metabolic programs to successfully colonize diverse microenvironment is poorly understood. Using an orthotopic xenograft mouse model of lung cancer that develops metastases and recapitulates metastatic lung cancer spread, we injected GFP-LUC-expressing human H1975 lung tumor cells into the left lungs of mice. In vivo bioluminescence imaging was used to visualize tumor growth and metastatic spread for 30 days. Animals were then euthanized and primary and metastatic tumors were collected from different anatomical sites of the body (left lung, right lung, mediastinum, abdominal metastases). Tumor samples were analysed by RNA sequencing analysis. The transcriptomes of lung metastases demonstrated a significant reduction in the expression of genes encoding respiratory pathway protein as compared to the primary lung tumors, suggesting metabolic reprogramming of their respiratory metabolism. CRISPRi-mediated silencing of genes encoding components of respiratory function in human lung cancer cells was associated with significantly increased metastatic spread in vivo. These studies suggest the functional importance of respiratory metabolism on modulating in vivo disease spread. Citation Format: Padmini Bisoyi, Yoshi Sei, Neal Bennett, Ken Nakamura, Jean L. Nakamura. Respiratory function linked to in vivo metastatic lung cancer progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5424.

  PublisherDOI

• Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production

  Zenodo (CERN European Organization for Nuclear Research) · 2023-10-13

  datasetOpen access1st authorCorresponding

  Dataset associated with publication "Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production"

  PublisherDOI

• Abstract 1161: Primary and metastatic tumors exhibit systems-level differences in dependence on mitochondrial respiratory function

  Cancer Research · 2023-04-04

  article1st authorCorresponding

  Abstract The Warburg effect, aerobic glycolysis, is a hallmark feature of cancer cells grown in culture. However, the relative roles of glycolysis and respiratory metabolism in supporting in vivo tumor growth and processes such as tumor dissemination and metastatic growth remain poorly understood, particularly on a systems level. Using a CRISPRi mini-library enriched for mitochondrial ribosomal protein and respiratory chain genes in multiple human lung cancer cell lines we analyzed in vivo metabolic requirements in xenograft tumors grown in distinct anatomic contexts. While knockdown of mitochondrial ribosomal protein and respiratory chain genes (mito-respiratory genes) has little impact on growth in vitro, tumor cells depend heavily on these genes when grown in vivo as either flank or primary orthotopic lung tumor xenografts. In contrast, respiratory function is comparatively dispensable for metastatic tumor growth. RNA-Seq and metabolomics analysis of tumor cells expressing individual sgRNAs against mito-respiratory genes indicate overexpression of glycolytic genes and increased sensitivity of glycolytic inhibition compared to control when grown in vitro, but when grown in vivo as primary tumors these cells downregulate glycolytic mechanisms. Metabolic shifts associated with silencing mito-respiratory genes can be detected in vivo with metabolic imaging. These studies demonstrate that discrete perturbations of mitochondrial respiratory chain function impact in vivo tumor growth in a context-specific manner with differential impacts on primary and metastatic tumors. Citation Format: Neal K. Bennett, Hiroki J. Nakaoka, Danny Laurent, Ross Okimoto, Yoshitaka Sei, Andrew E. Horvai, Trever G. Bivona, Georgios Batsios, Pavithra Viswanath, Johanna ten Hoeve, Thomas G. Graeber, Ken Nakamura, Jean L. Nakamura. Primary and metastatic tumors exhibit systems-level differences in dependence on mitochondrial respiratory function [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1161.

  PublisherDOI

• Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production

  Zenodo (CERN European Organization for Nuclear Research) · 2023-10-13

  datasetOpen access1st authorCorresponding

  Dataset associated with publication "Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production"

  PublisherDOI

• Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-10-18 · 3 citations

  preprintOpen access1st author

  Abstract Respiratory chain dysfunction can decrease ATP and increase reactive oxygen species (ROS) levels. Despite the importance of these metabolic parameters to a wide range of cellular functions and disease, we lack an integrated understanding of how they are differentially regulated. To address this question, we adapted a CRISPRi- and FACS-based platform to compare the effects of respiratory gene knockdown on ROS to their effects on ATP. Focusing on genes whose knockdown is known to decrease mitochondria-derived ATP, we showed that knockdown of genes in specific respiratory chain complexes (I, III and CoQ10 biosynthesis) increased ROS, whereas knockdown of other low ATP hits either had no impact (mitochondrial ribosomal proteins) or actually decreased ROS (complex IV). Moreover, although shifting metabolic conditions profoundly altered mitochondria-derived ATP levels, it had little impact on mitochondrial or cytosolic ROS. In addition, knockdown of a subset of complex I subunits—including NDUFA8, NDUFB4, and NDUFS8—decreased complex I activity, mitochondria-derived ATP and supercomplex level, but knockdown of these genes had differential effects on ROS. Conversely, we found an essential role for ether lipids in the dynamic regulation of mitochondrial ROS levels independent of ATP. Thus, our results identify specific metabolic regulators of cellular ATP and ROS balance that may help dissect the roles of these processes in disease and identify therapeutic strategies to independently target energy failure and oxidative stress. Significance Mitochondrial respiration generates both energy (ATP) and reactive oxygen species (ROS). Insufficient energy and increased ROS from respiratory chain dysfunction may be central to the pathophysiology of neurodegenerative diseases and aging. We established a screening platform using CRISPR and fluorescent-cell sorting to compare the impact of decreasing respiratory chain proteins on ROS and ATP levels. The results provide the first systems-level analysis of how ROS and ATP are differentially regulated, and identify genes and respiratory chain complexes that can manipulate each independently. These findings advance our understanding of the relative contributions of ATP and ROS to disease pathophysiology, and guide the development of therapies to preserve energy while minimizing ROS.

  PublisherOA PDFDOI

• Neurons require glucose uptake and glycolysis in vivo

  Cell Reports · 2023 · 125 citations

  • Chemistry
  • Cell biology
  • Biochemistry

  Neurons require large amounts of energy, but whether they can perform glycolysis or require glycolysis to maintain energy remains unclear. Using metabolomics, we show that human neurons do metabolize glucose through glycolysis and can rely on glycolysis to supply tricarboxylic acid (TCA) cycle metabolites. To investigate the requirement for glycolysis, we generated mice with postnatal deletion of either the dominant neuronal glucose transporter (GLUT3cKO) or the neuronal-enriched pyruvate kinase isoform (PKM1cKO) in CA1 and other hippocampal neurons. GLUT3cKO and PKM1cKO mice show age-dependent learning and memory deficits. Hyperpolarized magnetic resonance spectroscopic (MRS) imaging shows that female PKM1cKO mice have increased pyruvate-to-lactate conversion, whereas female GLUT3cKO mice have decreased conversion, body weight, and brain volume. GLUT3KO neurons also have decreased cytosolic glucose and ATP at nerve terminals, with spatial genomics and metabolomics revealing compensatory changes in mitochondrial bioenergetics and galactose metabolism. Therefore, neurons metabolize glucose through glycolysis in vivo and require glycolysis for normal function.

  PublisherOA PDFDOI

Recent grants

• Bioenergetic and Proteolytic Impact of Ubiquitin-like Pathways in Metabolically Stressed Neurons

  NIH · $155k · 2019–2022

Frequent coauthors

• Ken Nakamura

  Nippon Medical School

  31 shared

• Jean L. Nakamura

  University of California, San Francisco

  10 shared

• Prabhas V. Moghe

  Rutgers, The State University of New Jersey

  10 shared

• Martin Kampmann

  University of California, San Francisco

  9 shared

• Johanna ten Hoeve

  University of California, Los Angeles

  8 shared

• Adam L. Orr

  MIND Research Institute

  8 shared

• Thomas G. Graeber

  8 shared

• Hiroki J. Nakaoka

  8 shared

Awards & honors

• 2023 Outstanding Faculty Honor Award