Current Lab Members | Alumni

Principal Investigator

Hugo Bellen

Hugo Bellen
hbellen@bcm.edu
(713) 798-5272

Business Engineer, University of Brussels, Belgium
DVM, University of Ghent, Belgium
PhD, University of California, Davis

CVPubMed

Investigator, Howard Hughes Medical Institute, Baylor College of Medicine
Professor, Departments of Molecular and Human Genetics and Neuroscience
Director, Program in Developmental Biology

I am interested in (1) providing a better fundamental understanding of the biology that governs the proper function and maintenance of neurons in aging adults (2) developing tools that can be applied to most genes to control transcript and protein levels in adult neurons to assess which proteins are required for neuronal survival and proper function (3) creating genome wide libraries to manipulate most genes in vivo. My lab uses the fruit fly Drosophila melanogaster as a model system because most biological processes are evolutionarily conserved and studies in fruit flies provide many important clues about the aging process in animals and human diseases.

Lab Manager

Karen Schulze

Karen Schulze
kschulze@bcm.edu
(832) 824-8757

BS, Southwestern University
PhD, Baylor College of Medicine

Pubs

Assistant Professor

Manish Jaiswal

Manish Jaiswal
jaiswal@bcm.edu

BSc, APS University, India
MSc, DAVV University, India
PhD, Indian Institute of Technology, Kanpur, India (Pradip Sinha)

Pubs

Neurons are the longest lived cells in an organism. I am interested in understanding their survival mechanisms and use Drosophila visual system as a model. In a collaborative effort I performed a genetic screen on the X chromosome and identified numerous genes involved in the survival of photoreceptor neurons. Currently I am focusing on genes associated with mitochondrial function and affect survival of photoreceptor neurons.

Postdoctoral Fellows

Megan Campbell

Megan Campbell
megan.campbell@bcm.edu

BS, Gettysburg College
PhD, University of Wisconsin-Madison (Barry Ganetzky)

Pubs

Many genes involved in developmental pathways are expressed in post-mitotic cells; however their function at this stage is often unclear. I am interested in determining if these genes play a role in neuronal maintenance and if so, do they function in the canonical developmental pathway or through a novel mechanism to promote neuronal viability.

Hsiao-Tuan Chao

Hsiao-Tuan Chao
hc140077@bcm.edu

BS and BA, University of Texas at Austin
PhD, Baylor College of Medicine
MD, Baylor College of Medicine

Pubs

The advent of whole-exome and whole-genome sequencing has contributed to enormous advances in the diagnosis of rare diseases, with a large proportion of disease genes identified to impact the formation and function of the nervous system. However, with the rapid rate of disease gene discovery we are now faced with increasing numbers of rare variants identified in poorly characterized genes.

I am interested in utilizing human sequencing data and Drosophila melanogaster for high-throughout identification and analysis of the fundamental biology of novel genes mediating the pathogenesis of autism spectrum disorders with co-morbid epilepsy. In the absence of overt structural brain malformations, these disorders likely result from dysfunction on a microstructural or cellular level impacting circuit formation and synaptic transmission. Utilizing these disorders to identify pathogenic gene variants and gene networks will provide critical information regarding the formation of neural circuits, regulatory mechanisms of circuit function and synaptic transmission, and potentially open new avenues for therapeutic intervention.

Oguz Kanca

Oguz Kanca
oguz.kanca@bcm.edu

BS, Bilkent University, Ankara, Turkey
PhD, EMBL Heidelberg (Pernille Rørth)
Postdoc, Biozentrum, University of Basel (Markus Affolter)

Pubs

Whole exome sequencing and personalized medicine prompted the need for efficient methods to test the functionality of gene variants. I am interested in establishing techniques and tools to expedite the analysis of functionality of human gene variants, using the power of Drosophila genetics.

Pei-Tseng Lee

Pei-Tseng Lee
pei-tseng.lee@bcm.edu

BS, Taipei Medical College, Taiwan
MS, National Chung Hsing University, Taiwan
PhD, National Tsing Hua University, Taiwan (Ann-Shyn Chiang)

Pubs

Reactive oxygen species (ROS) are common by-products generated mostly in mitochondria. Excess ROS cause biomolecule damage and will further lead to neurodegeneration. Many neurodegenerative diseases like Alzheimer's disease, Parkinson's disease, multiple sclerosis and amyotrophic lateral sclerosis are exacerbated by ROS. Oxidative stress due to ROS also contributes to aging, a major risk factor for neurodegenerative diseases. By feeding fruit flies with paraquat, a poison known to increase ROS, we can screen mutants for sensitivity to ROS. This systemic screen allows us to address the cellular mechanisms involved in the response to ROS and increase and assess their contribution to neurodegeneration.

David Li-Kroeger

David Li-Kroeger
likroege@bcm.edu

BS, University of Cincinnati
MS, University of Cincinnati
PhD, University of Cincinnati (Brian Gebelein)

Pubs

For neurons, maintaining homeostasis in the face of accumulating stress is essential to prevent neurodegenerative diseases. In response to stress, neurons produce survival factors such as the NAD salvage enzyme Nicotinamide mononucleotide adenylyltransferase (Nmnat), which protects neurons from a variety of insults. For example, increased Nmnat protects severed axons from degeneration, protects neurons from chemotherapy agents, and reduces the aggregation of disease causing proteins like hyperphosphorylated Tau. While the varieties of conditions that can be ameliorated by Nmnat suggest a central role for this protein in cellular protection and/or survival, the mechanisms by which Nmnat protects neurons are not fully understood. The aim of my research is to use Drosophila genetics to gain mechanistic insight elucidating Nmnat function.

Guang Lin

Guang Lin
guangl@bcm.edu

BS, National Taiwan Ocean University
MS, National Taiwan Ocean University
PhD, Stony Brook University/CSHL (Nicholas Tonks)

Pubs

I am interested in studying the molecular function of genes that cause neurodegenerative diseases. In collaboration with other members in the lab, my research has focused on VAPB, frataxin and PLA2G6, which cause Amyotrophic Lateral Sclerosis (ALS), Friedreich's Ataxia (FA) and Neurodegeneration with brain iron accumulations (NBIAs), respectively. We have generated Drosophila loss-of-function mutations for each of them and are currently studying the phenotypes associated with loss of these genes. By studying the molecular mechanisms that underlie the identified phenotypes, we hope to gain insight in the clinical pathology of these neurodegenerative diseases.

Nichole Link

Nichole Link
nichole.link@bcm.edu

BA, Hendrix College
PhD, UT Southwestern Medical Center (John Abrams)

Pubs

Nuclear architecture and three-dimensional genome organization are important for maintaining proper gene regulation during development and differentiation. I am interested in the mechanisms that establish chromatin organization within the nucleus and how disruption of nuclear structure results in neuronal disorders.

Ning Liu

Ning Liu
ning.liu@bcm.edu

BS, Northeast Normal University, Changchun, China
MS, Jilin University, Changchun, China
PhD, University of Rochester, NY (Jeffrey Hayes)

Pubs

The development of Whole-Exome Sequencing (WES) and Whole-Genome Sequencing (WGS) provides powerful clinical diagnostic tools to identify novel disease genes and variants from patients with undiagnosed rare diseases. My research focuses on establishing and testing a pipeline for the characterization of human genes function using Drosophila as a model organism, further investigating the molecular and genetic mechanism by which human mutations lead to certain disease phenotypes. Also, I am interested in generating strategies and tools in Drosophila to determine the function of Autism Spectrum Disorders (ASD) candidate genes in the fly nervous system.

Xi Luo

Xi Luo
xi.luo@bcm.edu

BS, Nankai University, Tianjin, China
MS, University of Rochester, NY
PhD, Cornell University (Yuxin Mao)

Pubs

The Undiagnosed Diseases Network (UDN) aims to bring together clinical and research experts from across the United States to solve the most challenging medical mysteries using advanced technologies. The Simons Foundation Autism Research Initiative (SFARI) funds innovative research to improve the understanding, diagnosis and treatment of autism spectrum disorders. I am a member of the UDN-SFARI team at the Drosophila Core (DC) of the Model Organism Screening Center (MOSC). My goal is to take advantage of our cumulative knowledge and expertise as well as novel technologies and resources to provide in vivo functional information for evolutionarily conserved genes and determine the potential pathogenicity of variants found in UDN and SFARI patients. In addition, I am particularly interested in characterizing the importance of the patients' mutations in the protein structure to provide critical insights into the molecular mechanisms and biological pathways underlying human rare diseases.

Sathiyanarayanan Manivannan

Sathiyanarayanan Manivannan

B. Tech (Biotechnology), VIT (University), Vellore, Tamil Nadu, India
Ph.D, Ohio State University (Amanda Simcox)

Pubs

I am part of the Undiagnosed Diseases Network (UDN) team, working towards unraveling the genetic and molecular basis for diseases caused by yet unknown mechanisms. We are investigating Drosophila homologs of candidate genes and variants from patients, in order to dissect the role of those genes in basic cellular and organismal processes, as well as to understand how the mutation in the patient might lead to pathogenesis. I am also working as a part of the Simons Foundation Autism Research Initivate (SFARI) funded research to investigate genes in Drosophila, whose human orthologs have been implicated in Autism. I am interested in employing different assays and tools in Drosophila, in order to evaluate the contribution of different genes in neuronal processes, which ultimately affect their behavior.

Sonal Nagarkar-Jaiswal

Sonal Nagarkar-Jaiswal
snagarka@bcm.edu

BSc, Devi Ahilya University, India
MSc, Devi Ahilya University, India
PhD, University of Bayreuth, Germany (Stefan Heidmann)

Pubs

Tagging of endogenous genes with GFP provides a unique advantage to studying protein localization in vivo in live cells without overexpressing the gene. One of my goals is genome wide protein tagging using the MiMIC system developed in the Bellen lab to create a resource for the fly community. I am also generating new MiMIC based tools to knockout/knockdown genes in a temporal and spatial manner especially in adult neurons in Drosophila.

Hector Sandoval

Hector Sandoval
hectors@bcm.edu

BSc, Baylor University
PhD, Baylor College of Medicine (Jin Wang)

Pubs

Understanding mitochondrial fusion and fission function(s) in developing neurons. These fundamental cell biological processes control mitochondrial shape, number, size, distribution, and physiology. I am currently working on Drosophila homolog of Mitofusins role(s) in hormonal regulation of neuronal synaptic development.

Wan Hee Yoon

Wan Hee Yoon
whyoon@bcm.edu

BSc, Yonsei University, South Korea
MSc, Yonsei University, South Korea
PhD, Johns Hopkins University School of Medicine (Denise Montell)

Pubs

I am interested in understanding how dysregulation of metabolism contributes to human diseases - neurodegeneration and inborn errors of metabolism.
I am currently working on a mitochondrial gene whose loss leads to defects of metabolism and neuronal function. Taking advantage of fly and human genetics, I intend to extend my current study for identification of novel metabolic disease genes and understanding their functions.

Graduate Students

Kuchuan Chen

Kuchuan Chen
kuchuanc@bcm.edu

BS, National Tsing Hua University, Taiwan

Pubs

Loss of function of Frataxin (FXN) causes Friedreich's ataxia (FRDA), the most prevalent form of recessive cerebellar ataxia. The FXN protein is localized to the mitochondrial matrix, and its deficiency leads to impaired iron-sulfur (Fe-S) cluster biosynthesis and iron accumulation in the mitochondria. Although the mutation of FXN was identified 18 years ago, the pathological mechanism of FRDA is still unknown. In a forward genetic screen designed to identify mutations in genes that cause neurodegeneration in Drosophila, we isolated the first mutation in frataxin homolog (fh), a Drosophila homolog of mammalian FXN. Interestingly, fh mutants show age dependent photoreceptor degeneration. Currently we are investigating the mechanism of degeneration phenotype.

Nele Haelterman

Nele Haelterman
nhaelter@bcm.edu

BS, University of Leuven, Belgium
MS, University of Leuven, Belgium

Pubs

For our every movement, we depend on the coordinated function of neurons and their interaction with muscle cells. Developing the proper number of interactions between a motorneuron and its target muscle, called synapses, is critical to mediate muscle movement. I am interested in the molecular cues that are involved in developing these synapses between muscles and neurons. More specifically, I am studying the cues that control assembly and maintenance of active zones, the sites where neurotransmitter-containing synaptic vesicles are released from the neuron.

Tongchao Li

Tongchao Li
tongchal@bcm.edu

BS, Tsinghua University, China

Pubs

Hearing is an important peripheral sense and there are numerous human diseases linked to hearing defects. In the fly, normal hearing function plays a role in courtship and mating. The Drosophila auditory organ is named Johnston's Organ (JO), which contains chordotonal organs located in the second segment of antenna that are attached to the base of the third segment. The conservation of auditory organ development has been supported by previous studies. To identify essential genes that regulate the development of JO, I performed a mosaic genetic screen and identified multiple complementation groups exhibiting different defects in JO. One complementation group, XM35, shows the same phenotype as the mutant of Usher syndrome gene myo7a in JO. I am working on how XM35 regulates Myo7a and other Usher proteins.

Lucy Liu

Lucy Liu
lliu@cns.bcm.edu

BS, University of North Carolina at Chapel Hill

Pubs

I am interested in the role of lipid metabolism in the process of neurodegeneration. More specifically, I am currently determining how alterations in lipid metabolism contribute to the neurodegenerative process. To answer this question, I am using three neurodegenerative mutants isolated in the lab, all of which exhibit lipid droplet accumulation in the nervous system prior to signs of neurodegeneration. Currently, I am in the process of determining the mechanism by which alteration of lipid metabolism lead to neurodegeneration and translating what I have found in my three fly mutants into the vertebrate system using a knockout mouse via collaborations with another lab.

Dongxue Mao

Dongxue Mao
dmao@bcm.edu

BS, Tsinghua University, China

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects motor neurons, leading to muscle atrophy and paralysis. Mutations in VapB cause ALS, but the mechanism is unclear. I am interested in understanding the cellular functions of VapBin order to shed light on how loss of VapB can cause a motor neuron disease using Drosophila melanogaster.

Mumine Senturk

Mumine Senturk
senturk@bcm.edu

BS (Molecular Biology and Genetics), Bogazici University, Turkey
BS (Chemistry), Bogazici University, Turkey

Pubs

Genome-wide association studies have identified several integrin pathway components as Alzheimer's disease susceptibility loci. I am interested in identifying new players in the integrin signaling pathway and examining if these players function in neuronal maintenance and aging.
Integrins form strong adhesive junctions between tissue layers, a process that is required in the wing to keep the dorsal and ventral cells attached to each other. A loss of adhesion between these two epithelial layers causes wing blisters. To identify additional regulators of the integrin signaling pathway, we performed a morphological screen in the fly wing. Currently, I am investigating the role of one of the hits from the screen in fly nervous system.

Kai Li Tan

Kai Li Tan
ktan@bcm.edu

BS, Rutgers University

Pubs

Synaptic transmission is a complex process that involves various cellular activities, including but not limited to, protein synthesis and degradation, vesicular and protein trafficking, and fusion and fission of membranes. Orchestrating the different cellular activities is thus important to ensure optimal synaptic function. One key process that determines the efficiency of neuronal transmission is the tightly-regulated neurotransmitter release. My research focuses on how the formation and maintenance of active zones (neurotransmitter release sites) are regulated, in addition to identifying and understanding the mechanisms of novel components in regulating the exocytosis of neurotransmitter-containing vesicle.

Berrak Ugur

Berrak Ugur
ugur@bcm.edu

BS, Bogazici University, Turkey

Pubs

Mitochondria are essential for numerous biological processes including ATP production, fatty acid breakdown, Ca2+ homeostasis and Fe-S biogenesis. Hence dysfunction of any of these mitochondrial pathways can cause an exceptional phenotypic heterogeneity. To isolate genes that affect nervous system development, function and maintenance, we performed an unbiased, forward genetic screen for essential genes on the Drosophila X-chromosome and isolated 165 genes. 34 of the 165 genes encode mitochondrial proteins that are conserved in humans and loss of these genes in the fly causes multiple variable phenotypes. I am interested in identifying phenotypic patterns in mitochondrial mutants that will help us to understand underlying common molecular mechanisms by which mitochondrial dysfunction leads to neuronal demise and degeneration.

Julia Wang

Julia Wang
julia.wang@bcm.edu

BS, University of Michigan, Ann Arbor

Pubs

I am interested in combining patient genomic data with Drosophila genetics to understand fundamental biological processes.

The etiology of rare diseases is often unknown. Although sequencing data from these patients yield candidate genes, we often lack functional validation. Drosophila and its powerful genetic tools can efficiently validate the disease-causing genetic variants and allow us to pursue the underlying mechanisms of disease.

My project involves taking novel candidate disease causing genes from patients and determining pathogenic variants in Drosophila. Furthermore, because many of these candidates lack functional annotation, I hope to dissect their roles in basic biological mechanisms.

Research Technicians

Lita Duraine

Lita R. Duraine
duraine@bcm.edu
(832) 824-8704

Certified Electron Microscopist

Pubs

Yuchun He

Yuchun He
yhe@bcm.edu

Pubs

Hongling Pan

Hongling Pan
hpan@bcm.edu

Pubs

Zhongyuan Zuo

Zhongyuan (Zach) Zuo
zhongyuz@bcm.edu

BS, MS, University of Denver, CO

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Gene Disruption Project Team Technicians

Ying
Ying Fang
Qiaohong
Qiaohong Gao
Jianping
Jianping Li

Jiangxing Lv
Wen-Wen
Wen-Wen Lin
Lily
Lily Wang
Zhihua
Zhihua Wang
Jin
Jin Yue
Xue
Xue Zheng