PUBLICATION HIGHLIGHTS
From neurons and viruses to yeast and pathogenic fungi, our publications have challenged the idea that cell-death proteins act only during the final moments of a cell’s life. These selected studies highlight discoveries that have reshaped our understanding of infection, cellular energy, genome evolution, neurological disease, and microbial survival.
CELL SURVIVAL CAN CHANGE THE OUTCOME OF VIRAL INFECTION
Our early work demonstrated that the cellular protein BCL-2 could shift alphavirus infection in the brain from destructive cell lysis toward persistent infection. This established that host cell-death machinery can help determine both viral pathogenesis and disease outcome.
WHEN PROTECTORS BECOME KILLERS
We discovered that caspases can cleave the normally protective BCL-2 protein and transform it into a Bax-like promoter of cell death. Subsequent studies showed that viral BCL-2 homologs follow different rules, escaping this conversion while manipulating the survival machinery of infected cells.
Cheng EHY, et al. “Conversion of Bcl-2 to a Bax-like death effector by caspases.” Science, 1997.
THE HIDDEN “DAY JOBS” OF CELL-DEATH PROTEINS
Our research helped establish that BCL-2 family proteins perform essential functions long before apoptosis begins. Studies of BCL-xL revealed roles in neuronal energy efficiency, mitochondrial physiology, membrane organization, and cellular adaptation to changing energy demands.
ONE GENE DELETION CAN RESHAPE A GENOME
A genome-wide analysis in baker’s yeast revealed that deleting a single gene frequently selects for a second, compensatory mutation. This discovery exposed a hidden layer of genome adaptation with broad implications for experimental genetics and the earliest stages of tumor evolution.
Teng X, et al. “Genome-wide consequences of deleting any single gene.” Molecular Cell, 2013.
FROM YEAST GENETICS TO HUMAN NEURODEGENERATION
Cross-species studies connected KCTD7 deficiency to conserved defects in autophagy and lysosomal function. This work defined a distinct neurodegenerative disorder and demonstrated how discoveries in simple model organisms can reveal mechanisms underlying severe human disease.
MAPPING CELL DEATH IN YEAST AND PATHOGENIC FUNGI
We defined an AP-3-dependent yeast cell-death pathway that culminates in vacuole/lysosome membrane permeabilization. Building on this work, the lab developed a heat-ramp method for measuring regulated cell death in Cryptococcus neoformans, creating new tools for investigating fungal survival, virulence, and potential therapeutic vulnerabilities.