基本信息
浏览量:29
职业迁徙
个人简介
Research
Our work spans the areas of cell biology, genetics, neurobiology and biochemistry. We have two independent research projects that superficially are very different, but that converge on similar techniques and cell biological questions related to vesicular trafficking.
Neuromodulation
In one project, we seek to understand the molecular mechanisms of neuromodulation. Neuromodulators are typically neuropeptides, or monoamines such as dopamine, noradrenaline, and serotonin. The release of neuromodulators from dense-core vesicles affects our moods, emotions and appetites. However, dense-core vesicle biogenesis, trafficking and release are not well understood, primarily because few molecules specific to dense-core vesicle function have been identified. Using a genetic screen in C. elegans, we identified at least six novel conserved molecules that function in dense-core vesicle trafficking. One of these encodes a protein with a RUN domain. We have shown that this protein interacts with the small GTPase Rab2 through its RUN domain and functions as a Rab2 effector in the maturation of dense-core vesicles at the trans-Golgi network. Our future plans aim at further dissecting the mechanism of action of these proteins and determining the function of the other new proteins we’ve identified.
Genetic Incompatibilities
In our second project, we are investigating the cellular mechanism of action of a novel selfish genetic element that mediates hybrid incompatibility between different strains of C. elegans. The element consists of a dominant paternal-effect gene peel-1 that acts as a toxin, and its zygotically-acting antidote zeel-1. peel-1 encodes a novel transmembrane protein that is expressed in sperm and delivered to the embryo via specialized, sperm-specific vesicles. In the absence of zeel-1, sperm-supplied PEEL-1 causes lethal defects at a surprisingly late stage of embryogenesis. Remarkably, ectopically expressed PEEL-1 is a potent cytotoxin that kills a variety of cell types, and ectopic ZEEL-1 can rescue this killing. Our future plans aim to determine the mechanism of PEEL-1 toxicity and how ZEEL-1 rescues the toxicity. We also would like to determine whether PEEL-1 is cytotoxic in other organisms because PEEL-1 could be useful as a tool for cell-specific ablation, as well as having possible therapeutic applications.
This study of genetic incompatibilities initially stemmed from a hope to identify genes involved in incipient speciation events. We are still interested in speciation and have been actively involved in isolating new species and wild isolates of Caenorhabditis in the hopes of finding new model systems to study the genetics of incompatibility.
Our work spans the areas of cell biology, genetics, neurobiology and biochemistry. We have two independent research projects that superficially are very different, but that converge on similar techniques and cell biological questions related to vesicular trafficking.
Neuromodulation
In one project, we seek to understand the molecular mechanisms of neuromodulation. Neuromodulators are typically neuropeptides, or monoamines such as dopamine, noradrenaline, and serotonin. The release of neuromodulators from dense-core vesicles affects our moods, emotions and appetites. However, dense-core vesicle biogenesis, trafficking and release are not well understood, primarily because few molecules specific to dense-core vesicle function have been identified. Using a genetic screen in C. elegans, we identified at least six novel conserved molecules that function in dense-core vesicle trafficking. One of these encodes a protein with a RUN domain. We have shown that this protein interacts with the small GTPase Rab2 through its RUN domain and functions as a Rab2 effector in the maturation of dense-core vesicles at the trans-Golgi network. Our future plans aim at further dissecting the mechanism of action of these proteins and determining the function of the other new proteins we’ve identified.
Genetic Incompatibilities
In our second project, we are investigating the cellular mechanism of action of a novel selfish genetic element that mediates hybrid incompatibility between different strains of C. elegans. The element consists of a dominant paternal-effect gene peel-1 that acts as a toxin, and its zygotically-acting antidote zeel-1. peel-1 encodes a novel transmembrane protein that is expressed in sperm and delivered to the embryo via specialized, sperm-specific vesicles. In the absence of zeel-1, sperm-supplied PEEL-1 causes lethal defects at a surprisingly late stage of embryogenesis. Remarkably, ectopically expressed PEEL-1 is a potent cytotoxin that kills a variety of cell types, and ectopic ZEEL-1 can rescue this killing. Our future plans aim to determine the mechanism of PEEL-1 toxicity and how ZEEL-1 rescues the toxicity. We also would like to determine whether PEEL-1 is cytotoxic in other organisms because PEEL-1 could be useful as a tool for cell-specific ablation, as well as having possible therapeutic applications.
This study of genetic incompatibilities initially stemmed from a hope to identify genes involved in incipient speciation events. We are still interested in speciation and have been actively involved in isolating new species and wild isolates of Caenorhabditis in the hopes of finding new model systems to study the genetics of incompatibility.
研究兴趣
论文共 76 篇作者统计合作学者相似作者
按年份排序按引用量排序主题筛选期刊级别筛选合作者筛选合作机构筛选
时间
引用量
主题
期刊级别
合作者
合作机构
Biology openno. 7 (2023)
bioRxiv (Cold Spring Harbor Laboratory) (2023)
引用0浏览0引用
0
0
microPublication biology (2023)
引用0浏览0WOS引用
0
0
bioRxiv : the preprint server for biology (2023)
加载更多
作者统计
合作学者
合作机构
D-Core
- 合作者
- 学生
- 导师
数据免责声明
页面数据均来自互联网公开来源、合作出版商和通过AI技术自动分析结果,我们不对页面数据的有效性、准确性、正确性、可靠性、完整性和及时性做出任何承诺和保证。若有疑问,可以通过电子邮件方式联系我们:report@aminer.cn