Akihiro Ikeda
Associate Professor of Medical Genetics
Ph.D., University of Tokyo, 1997
Postdoctoral Research: The Jackson Laboratory, 1997-2003
Address: 5322 Genetics/Biotech
Telephone: 262-5477
E-mail: aikeda@wisc.edu
Research Interests:
Mouse genetics, development and function of the synapse, sensory neuronal disease
Research Fields:
Mouse Genetics
Molecular Genetics
Neurogenetics
Research Description: Our research program is divided into two broad areas aimed at understanding the genetic and molecular mechanisms that regulate (1) synaptic interactions between neurons and (2) control of cell proliferation. Both processes involve fundamental biological questions that remain to be solved and both have important connections with human disease. The experimental system for most of our studies is the mouse eye, which offers a number of advantages: The eye is not a vital organ so mutations affecting the processes of interest can be identified and studied throughout the entire span of development. The well-organized structure and easy accessibility of the eye facilitate experimental analyses. At the same time, because the cells present in the eye (e. g. epithelial cells, neurons) are representative of cell types present in other organs, information gained from studies on the eye can reveal cellular mechanisms of general significance. Our studies of synaptic interactions are also carried out on mouse cerebellum because of its regular synaptic organization and because mutations affecting cerebellum can be readily identified by screening for defects in motor control. In general, our studies utilize a forward genetic approach, beginning with mutants that manifest phenotypes of interest. A major advantage of this phenotype-driven approach is that it offers the potential of identifying previously unknown genes and molecular pathways that regulate a process of interest. After a gene/protein of interest has been identified, we aim to unravel the pathway by which it normally acts whose disruption results in the observed phenotype. One major approach we use in dissecting these pathways is to identify genetic modifiers that interact with the original mutation indicating that they are likely to be affecting other components in the same pathway. In this way, we can expand beyond the original mutation to obtain additional entry points into the same pathway and allow a more complete understanding of the molecular pathways that underlie the phenotypes under investigation.
Over the past years, we have used these approaches to identify and characterize several genes of interest and to begin to elucidate the pathways through which they operate. Our immediate future goals are to obtain a more detailed understanding of these pathways to advance our understanding of the mechanisms that regulate synaptic development and maintenance and cell proliferation.
Representative Publications:
Verdoni A, Schuster KJ, Cole BS, Ikeda A, Kao WW, Ikeda S. 2010. Deletion of Serum Response Factor Rescues the Cornea Defects Caused by the Loss of Actin Depolymerizing Factor (ADF/Destrin) in Mouse. Genetics (in press)
Xu X, Kedlaya R, Higuchi H, Ikeda S, Justice MJ, Setaluri V, Ikeda A. 2010. Mutation in Archain 1, a Subunit of COPI Coatomer Complex, Causes Diluted Coat Color and Purkinje Cell Degeneration. PLoS Genet 6(5): e1000956.
Verdoni A, Ikeda S, Ikeda A. 2010. Deletion of serum response factor in developing skin epithelium leads to defects in barrier function, cytoskeletal organization, and epithelial sheet formation. Mamm Genome. 21:64-76.
Verdoni AM, Aoyama N, Ikeda A, Ikeda S. 2008. The effect of destrin mutations on the gene expression profile in vivo. Physiol Genomics. 34:9–21.
Johnson BA, Aoyama N, Friedell NH, Ikeda S, Ikeda A. 2008. Genetic Modification of the Schisis Phenotype in a Mouse Model of X-Linked Retinoschisis. Genetics. 178: 1785-94.
Associate Professor of Medical Genetics
Ph.D., University of Tokyo, 1997
Postdoctoral Research: The Jackson Laboratory, 1997-2003
Address: 5322 Genetics/Biotech
Telephone: 262-5477
E-mail: aikeda@wisc.edu
Research Interests:
Mouse genetics, development and function of the synapse, sensory neuronal disease
Research Fields:
Mouse Genetics
Molecular Genetics
Neurogenetics
Our research program is divided into two broad areas aimed at understanding the genetic and molecular mechanisms that regulate (1) synaptic interactions between neurons and (2) control of cell proliferation. Both processes involve fundamental biological questions that remain to be solved and both have important connections with human disease. The experimental system for most of our studies is the mouse eye, which offers a number of advantages: The eye is not a vital organ so mutations affecting the processes of interest can be identified and studied throughout the entire span of development. The well-organized structure and easy accessibility of the eye facilitate experimental analyses. At the same time, because the cells present in the eye (e. g. epithelial cells, neurons) are representative of cell types present in other organs, information gained from studies on the eye can reveal cellular mechanisms of general significance. Our studies of synaptic interactions are also carried out on mouse cerebellum because of its regular synaptic organization and because mutations affecting cerebellum can be readily identified by screening for defects in motor control. In general, our studies utilize a forward genetic approach, beginning with mutants that manifest phenotypes of interest. A major advantage of this phenotype-driven approach is that it offers the potential of identifying previously unknown genes and molecular pathways that regulate a process of interest. After a gene/protein of interest has been identified, we aim to unravel the pathway by which it normally acts whose disruption results in the observed phenotype. One major approach we use in dissecting these pathways is to identify genetic modifiers that interact with the original mutation indicating that they are likely to be affecting other components in the same pathway. In this way, we can expand beyond the original mutation to obtain additional entry points into the same pathway and allow a more complete understanding of the molecular pathways that underlie the phenotypes under investigation. Over the past years, we have used these approaches to identify and characterize several genes of interest and to begin to elucidate the pathways through which they operate. Our immediate future goals are to obtain a more detailed understanding of these pathways to advance our understanding of the mechanisms that regulate synaptic development and maintenance and cell proliferation.
Verdoni A, Schuster KJ, Cole BS, Ikeda A, Kao WW, Ikeda S. 2010. Deletion of Serum Response Factor Rescues the Cornea Defects Caused by the Loss of Actin Depolymerizing Factor (ADF/Destrin) in Mouse. Genetics (in press)
Xu X, Kedlaya R, Higuchi H, Ikeda S, Justice MJ, Setaluri V, Ikeda A. 2010. Mutation in Archain 1, a Subunit of COPI Coatomer Complex, Causes Diluted Coat Color and Purkinje Cell Degeneration. PLoS Genet 6(5): e1000956.
Verdoni A, Ikeda S, Ikeda A. 2010. Deletion of serum response factor in developing skin epithelium leads to defects in barrier function, cytoskeletal organization, and epithelial sheet formation. Mamm Genome. 21:64-76.
Verdoni AM, Aoyama N, Ikeda A, Ikeda S. 2008. The effect of destrin mutations on the gene expression profile in vivo. Physiol Genomics. 34:9–21.
Johnson BA, Aoyama N, Friedell NH, Ikeda S, Ikeda A. 2008. Genetic Modification of the Schisis Phenotype in a Mouse Model of X-Linked Retinoschisis. Genetics. 178: 1785-94.
