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 & Human Genetics and Neuroscience, and 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

Postdoctoral Fellows

Scott Barish

Scott Barish
scott.barish@bcm.edu

BS, Hampshire College
PhD, Duke University

Pubs

I am interested in modeling disease to uncover the fundamental mechanisms of neuronal biology. Currently, I use the fly eye as model for Alzheimer's Disease to understand how neurons age and respond to oxidative stress. Our lab has shown that oxidative stress causes neurons to produce peroxidated lipids that are shuttles to nearby glial cells and packaged into lipid droplets. In order to better understand this pathway, I am investigating known Alzheimer's Disease risk genes that may be involved in lipid export from neurons. I am also working to understand how chromatin modifying proteins lead to neurodevelopmental disorders.

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.

Hyunglok Chung

Hyunglok Chung
hyunglok.chung@bcm.edu

BS, KAIST, Republic of Korea
PhD, KAIST, Republic of Korea

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. As one of my projects, I am investigating the DMXL1 human gene and its variants identified by Whole-Genome Sequencing (WGS) in a UDN patient. I will determine the potential pathogenicity of DMXL1 variants found in the patient and explore the molecular functions of Rabconnectin-3a, the fly homologue.

In addition, as I am particularly interested in the genes associated with developmental signaling pathways such as Hippo (Hpo), Hedgehog (Hh) and Wingless (Wg), I will focus on the UDN cases relevant to these pathways. I am eager to discover the mechanisms by which the variants affect these developmental signaling pathways and mediate the pathogenesis of these rare human diseases.

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.

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.

Dongxue Mao

Dongxue Mao
dmao@bcm.edu

BS, Tsinghua University, China
PhD, Baylor College of Medicine

Pubs

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.

Paul Marcogliese

Paul Marcogliese
paul.marcogliese@bcm.edu

BS and BA, Carleton University, Canada
PhD, University of Ottawa, Canada

Pubs

I am interested in the discovery and characterization of novel genes involved in a variety of undefined neurological conditions. In attempts to streamline these efforts, I am part of the Undiagnosed Diseases Network (UDN). The UDN uses next-generation sequencing (whole-genome and whole-exome) to determine causative gene variants in these patients. This is followed by rapid generation of Drosophila with strong loss of function alleles in these genes. The characterization of these flies and further examination of the underlying molecular and cellular mechanisms underlying the phenotype in flies may provide vital insight into the human disease.

Matthew Moulton

Matthew Moulton

BS, Brigham Young University
PhD, University of Utah

Pubs

Research into Alzheimer's disease (AD) has led to the identification of key molecular players in the etiology and pathogenesis of the disease. However, despite tremendous efforts, few effective therapeutic options are available for AD patients. In an effort to identify gene candidates that might prove useful for therapeutic intervention, I seek to better understand the molecular underpinnings of AD. Our lab has demonstrated that proper lipid generation and storage is critical for healthy brain function. While it is clear that under stress conditions, neurons produce lipids that are exported and endocytosed by glia to make lipid droplets (LDs), we do not know all the genes involved in this neuron-to-glia shuttling of lipids. I am undertaking an effort to identify these genes and examine their role in LD formation and clearance of the neurotoxic molecule Aβ42. Aβ42, a protein fragment produced by cleavage of APP, is lipophilic and we predict that it can be endocytosed through the same pathway used to endocytose lipids potentially leading to its sequestration and/or degradation. Thus, the formation of LDs may be beneficial in sequestering toxic species of lipids and proteins and an important pathway to consider for the development AD therapies.

Mumine Senturk

Mumine Senturk
senturk@bcm.edu

BS (Molecular Biology and Genetics), Bogazici University, Turkey
BS (Chemistry), Bogazici University, Turkey
PhD, Baylor College of Medicine

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.

Graduate Students

Thomas Ravenscroft

Thomas Ravenscroft
thomas.ravenscroft@bcm.edu

BSc, The University of Manchester

Pubs

Neurodegenerative diseases arrise from a multitude of different causes, and can originate in various locations within the nervous system to cause harm. I am interested in understanding what causes certain neuronal populations to have an increased vulnerability to different insults whether they be genetic or environmental. Using the exciting genetic tools at our disposal in Drosophila melanogaster, I aim to learn more about the variances between neuronal populations in terms of their architecture, composition and physiology. Using a common component of all neurons, the sodium channel gene para, and selective targeting of neurons using the UAS-GAL4 system, I aim to identify the components that are unique to specific neurons as well as the consequences when these neurons are depleted.

Jose Salazar

Jose Salazar
jose.salazar@bcm.edu

BS (Horticulture), Texas A&M University

Pubs

Alzheimer's disease (AD) affects millions of people in the United States alone. Although genes and mutations that cause early-onset AD have been studied extensively, genetic risk factors of late-onset AD are less understood. I am interested in uncovering the molecular function of TM2D3, a new late-onset AD risk gene, and its related homologs to unravel novel cellular pathways that predispose individuals to AD and related neurodegenerative disorders.

I am co-mentored by Shinya Yamamoto.

Burak Tepe

Burak Tepe
tepe@bcm.edu

BSc, Bogazici University, Turkey

Pubs

Friedreich's ataxia (FRDA) is the most prevalent form of recessive cerebellar ataxia and it is caused by mutations in Frataxin (FXN). Frataxin (FXN) is required for normal mitochondrial function and intracellular iron homeostasis. We have recently shown a mitochondria independent pathway through iron accumulation, sphingolipid synthesis and ectopic activation of the PDK1/Mef2 signaling leading to neurodegeneration in both Drosophila and mouse models. Currently I am investigating therapeutic potential of manipulating the sphingolipid/PDK1 pathway to suppress the neurodegenerative features caused by loss of FXN.

I am co-mentored by Ben Arenkiel.

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.

Liping Wang

Liping Wang

BS, Shanghai Ocean University, China
MS, University of Southern California, Los Angeles

Pubs

The role of sphingolipid metabolism and endolysosomal dysfunction in neurodegenerative diseases, including Parkinson's disease (PD), is not well understood. My research is focused on the mitochondrial protein Pink1, retromer components Vps26, Vps29, and Vps35, and phospholipase PLA2G6, which are all implicated in PD or Parkinsonism. By utilizing genetic recombinase and the T2A-Gal4 system, I seek to understand sphingolipid metabolism alterations induced by loss of each of these genes. By understanding sphingolipid metabolism alterations in PD-associated mutants, I hope to discover novel pathogenic pathways of PD.

Research Technicians

Electron Microscopy

Lita Duraine

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

Certified Electron Microscopist

Pubs

Zhongyuan Zuo

Zhongyuan (Zach) Zuo
zhongyuz@bcm.edu

BS, MS, University of Denver, CO

Pubs

Lab Technicians

Hema Bhavana

Hema Bhavana
bhavana@bcm.edu

Pubs

Fatima Fazal

Fatima Fazal
fazal@bcm.edu

MBBS, Ziauddin Medical University, Karachi, Pakistan

Jake Harland

Jake Harland
harland@bcm.edu

BSc, Kings College London

Gene Disruption Project Team Technicians

Ming Ge

Ming Ge
mge@bcm.edu

Pubs

Yuchun He

Yuchun He
yhe@bcm.edu

Pubs

Wen-Wen Lin

Wen-Wen Lin
wenwenl@bcm.edu

BS, MS, National Taiwan Ocean University

Pubs

Hongling Pan

Hongling Pan
hpan@bcm.edu

MD, Xinjiang Medical University, China

Pubs


Junyan Fang
Junyan Fang
Ying Fang
Ying Fang
Liwen Ma
Liwen Ma
Lily Wang
Lily Wang
Zhihua Wang
Zhihua Wang
Ruifang Zhang
Yaping Yu
Jin Yue
Jin Yue
Ruifang Zhang
Ruifang Zhang
Xue Zheng
Xue Zheng