News

20262025202420232022

Lynne Maquat honored with Steven C. Beering Award

Friday, October 23, 2026

Lynne Maquat, the J. Lowell Orbison Endowed Chair and Professor in the Department of Biochemistry and Biophysics, director of the University of Rochester Medicine Center for RNA Biology, and co-director of the New York State Center of Excellence in RNA Research and Therapeutics (CERRT), is the winner of the 2026 Steven C. Beering Award for the Advancement of Biomedical Research from the Indiana University School of Medicine. Honored for her research on RNA mechanisms that contribute to a wide range of diseases, Maquat’s work has laid the foundation for the development of treatments targeting conditions that can’t be corrected with conventional drugs. Learn more.

Prenatal Iron Deficiency Leaves Lasting Changes in The Developing Brain

Tuesday, October 20, 2026

Published in The Journal of Nutrition, the study by the professor of Biomedical Genetics and Neuroscience found that supplementation restored blood iron levels, but deficiencies and imbalances in iron and other essential minerals persisted in the brain. Researchers also identified lasting changes in gene expression and neural networks involved in brain development, communication, and sensory processing.

Vera Gorbunova Pinpoints Surprising Role for Aging-Linked Protein

Wednesday, September 16, 2026

Until now, researchers believed that shutting down the cGAS protein could slow aging. But in a Nature Aging paper, the professor of Biology and her team discovered the opposite: Removing cGAS made mice age faster.

The findings suggest that cGAS has contradictory roles, and understanding them could impact therapies designed to reduce age-related inflammation.

Dakarai Esgadaille Defends His Thesis!

Monday, September 14, 2026

On September 14, 2026, BGG student Dakarai Esgadaille successfully defended his doctoral thesis. Dakarai joined BGG PhD program in fall of 2019 and joined Dr. Stephano's and Paul Boutz's lab in fall of 2020. His research involves understanding the mechanism of pre-mRNA splicing regulation by the long non-coding RNA Neat1.

Congratulations, Dr. Dakarai Esgadaille!

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with poor patient outcomes, often due to the development of drug resistance. Shifts in tumor cell transcriptional subtypes from well-differentiated classical to poorly differentiated basal-like cells can drive PDAC chemotherapeutic resistance. Such transcriptomic changes have been linked to cellular metabolic states, but how coordination of transcriptional and metabolic programs is mediated at the molecular level remains unclear. The stress-responsive long non-coding RNA NEAT1, an essential constituent of nuclear condensates called paraspeckles, has been associated with classical PDAC and was previously linked to regulation of cellular metabolism. In this study, we utilized a high throughput drug screening approach in NEAT1-deficient cancer cells to uncover functional metabolic targets in these cells, identifying ferroptosis via GPX4 inhibition as a major vulnerability of cells lacking paraspeckles. We find that the paraspeckle-forming isoform of NEAT1 is central to ferroptosis suppression and we extend these results into PDAC cell line models with genetic suppression and activation of NEAT1. We find that NEAT1-nucleated paraspeckles underlie the expression program tied to classical PDAC subtype and promote ferroptosis resistance. We pinpoint the paraspeckle suppressive RNA-binding protein QKI, associated with basal-like PDAC, as a positive regulator of ferroptosis susceptibility, possibly through its suppression of paraspeckles. These results link NEAT1 and regulation of paraspeckle condensates to subtype-specific ferroptosis susceptibility in PDAC and offer novel avenues for targeting metabolic vulnerabilities of pancreatic cancer cells on the basis of transcriptional subtype.

Zach Ward Defends His Thesis!

Tuesday, September 8, 2026

On September 8, 2026, BGG student Zach Ward successfully defended his doctoral thesis. Zach joined BGG PhD program in fall of 2020 and joined Dr. Andrew Samuelson's lab in fall of 2021. After a couple of years in Samuelson's lab, Zach decided to head in a different direction and joined Dr. Portman's lab in fall of 2023. His research involves the genetic programs sexually dimorphic behaviors in C. elegans.

Congratulations, Dr. Zach Ward!

Abstract: Sexual dimorphism in the nervous system, pervasive throughout animals, remains poorly understood, both in its developmental origins and in its e\ects. In C. elegans, one e\ect of biological sex is to modulate the function of sex-shared neurons. For example, the ADF neurons, which are born in the embryo and are present in both sexes, become sensitive to ascaroside sex pheromones only in adult males. This provides an opportunity to understand the molecular mechanisms by which a fully di\erentiated neuron can be functionally reprogrammed by biological sex during sexual maturation.

Using an RNA-seq-based approach, we identified four chemoreceptor genes (srd-58, srd-59, srx-42, and srx-88) that are expressed exclusively in ADF, and only in adult males. To understand the molecular basis for this specificity (neuronal identity, sexual state, and developmental stage), we focused on srd-59. ADF-specific feminization or masculinization was su\icient to turn srd-59 o\ or on, respectively, indicating that master sexual regulator TRA-1A acts in ADF to impart sex-specificity. Unexpectedly, srd-59 expression did not require the known ADF sexual e\ector gene mab-3, but did depend on lin-29a, another integrator of biological sex and developmental stage.

To understand how srd-59 integrates three dimensions of regulation, we carried out promoter dissection studies. These uncovered a compact, ~40-bp region su\icient to recapitulate adult-specific, male-specific, and ADF-specific gene expression. This region contains no candidate binding site for LIN-29A, but does harbor a site for LAG-1, a known ADF "terminal selector." Disrupting this site abolished expression of the srd-59 reporter, as did pan-neuronal degradation of AID::LAG-1. We also identified candidate LAG-1 sites in the other adult male ADF chemoreceptors and confirmed their necessity.

Because LAG-1 actively promotes expression of the serotonin biosynthesis gene tph-1 in ADF throughout development and in both sexes and throughout development, we hypothesized that another factor might impart sex and adult-specificity to LAG-1 in the minimal ~40-bp region. Interestingly, we identified a short motif located near the LAG-1 sites of srd-58/59, srx-42, and srx-88, but not in tph-1 or other serotonergic markers. Disrupting this auxiliary site also abolished expression in all cases tested. Excitingly, swapping the peri-LAG-1 region from srd-59 into a tph-1 reporter made its expression in ADF male-specific.

The sequence of this second cis-regulatory element suggested that it recruits the transcription factor NHR-6, the C. elegans ortholog of the vertebrate NR4A nuclear hormone receptor family. Using loss-of-function alleles and ectopic overexpression of nhr-6 in hermaphrodites, we found that nhr-6 is both necessary and su\icient to activate the male-specific transcriptional program in ADF. Together, these findings uncover a transcriptional mechanism in which the cell identity factor LAG-1 cooperates with the male-enriched transcription factor NHR-6 at male-specific chemosensory promoters to drive male-specific GPCR expression.

Ruchira Singh Finds Early Cause of Vision Loss in Batten Disease

Wednesday, August 26, 2026

Researchers have developed a new way to study CLN3-Batten disease, a rare, inherited condition that causes early vision loss in children followed by progressive neurological decline. Their findings offer new insight into how the disease begins and point to a promising path for treatment.

Vision loss is often the first and most life-altering symptom for children with the disease, affecting their ability to read, learn, and navigate the world independently, often years before other neurological symptoms appear.

Studying CLN3-Batten disease has been challenging because the earliest damage occurs deep within the retina, a part of the eye that is difficult for researchers to access. To overcome this, researchers at University of Rochester Medicine have created a 3D human stem cell-derived retina model that closely mimics how key parts of the eye work together, specifically, the interaction between light-sensing photoreceptors and support cells called the retinal pigment epithelium (RPE).

“Although molecular and cellular changes associated with the disease have been shown in other models, this retina model captures the earliest and most consistent pathology seen in patients, including photoreceptor outer segment loss and degeneration,” said Ruchira Singh, PhD, an associate professor in the URochester Medicine Flaum Eye Institute, and lead author of the study, which appears in Science Translational Medicine.

Alaa Ahmed Defends Her Thesis!

Wednesday, July 15, 2026

On July 15, 2026, BGG student Alaa Abdelmageed Ahmed successfully defended her doctoral thesis. Alaa joined BGG PhD program in fall of 2020 and joined Dr. Stephen Dewhurst’s lab in fall of 2021. Her research has involved deciphering the underlying mechanisms of resistance by some Cancer cells.

Congratulations, Dr. Alaa Abdelmageed Ahmed!

Abstract:
Cancer cells often have defects in antiviral pathways, making them susceptible to oncolytic viruses like vesicular stomatitis virus (VSV). However, some cancer cells resist viral infection through the constitutive expression of interferon-stimulated genes. This research explored the role of NF-κB activation and NF-κB-dependent antiviral signaling in establishing resistance to VSV infection in the PC3 cell line, derived from an aggressive metastatic prostate cancer (PrCa) tumor. Results confirm that multiple steps in the NF-κB pathway are differentially activated in PC3 and the VSV-susceptible LNCaP cells. Analysis using transcriptomics and proteomics approaches was conducted to further understand pathway-pathway interactions with the NF-κB pathway leading to the VSV-resistance phenotype. Additionally, this research highlights the differential expression of the BCL-2 gene and other apoptosis proteins in this resistance, which can be reversed by blocking BCL-2 expression. Onco-virotherapy using VSV is a promising tool in cancer therapeutics yet enhancing the tumor-killing capability of the virus in resistant cells will result in better treatment outcomes in a clinical setting.

Congratulations, Dr. McKayla Ford!

Monday, May 18, 2026

On May 18, 2026 BGG student McKayla Ford successfully defended her doctoral thesis. McKayla Joined BGG PhD program in 2020 and Dr. Paula Vertino's lab in the fall of 2021. Her research has involved dissection of the relationship between DNA sequence, DNA structure and transcriptional dynamics.

Abstract:
To control gene expression and allow for differentiation, regulation of the transcriptional process is vital. CpG islands (CGI), regulatory regions within DNA with a specific sequence and chromatin signature, support transcription by acting as promoters and enhancers. In this dissertation, the role of CpG islands in the regulation of transcription is examined, with a specific focus on the impact of the transition from CGI to non-CGI DNA has on early elongation. Sequence and structural characteristics of the CGI are also studied throughout this work in relation to their connection to transcription

Isaac Harris, Ph.D. publishes paper on 'Catabolism of extracellular glutathione supplies cysteine to support tumours' in Nature

Friday, March 27, 2026

​

Recently, BGG Program Director, Isaac Harris published a paper in Nature on “Catabolism of extracellular glutathione supplies cysteine to support tumours”.

Abstract:
Restricting amino acids from tumours is an emerging therapeutic strategy with substantial promise1. Although typically considered an intracellular antioxidant with tumour-promoting capabilities2, glutathione (GSH), as a tripeptide of cysteine, glutamate and glycine, can be catabolized to release amino acids. The extent to which GSH-derived amino acids are essential to cancers is unclear. Here we show that depletion of intracellular GSH does not alter tumour growth and extracellular GSH is highly abundant in the tumour microenvironment, highlighting the potential importance of GSH outside tumours. Supplementation with GSH rescues cancer cell survival and growth in cystine-deficient conditions, and this rescue depends on the catabolic activity of γ-glutamyltransferases. Finally, pharmacological targeting of the activity of γ-glutamyltransferases prevents the breakdown of circulating GSH, reduces tumour cysteine levels and slows tumour growth. Our findings indicate a non-canonical role for GSH in supporting tumours by acting as a reservoir of amino acids. Depriving tumours of extracellular GSH or inhibiting its breakdown is potentially a therapeutically tractable approach for patients with cancer. Furthermore, these findings change our view of GSH and how amino acids, including cysteine, are supplied to cells.