Matthew J. Anderson, Ph.D.
- Center for Cancer Research
- National Cancer Institute
- Building 560, Room 21-11
- Frederick, MD 21702-1201
Dr. Anderson uses complex mouse genetics and advanced imaging analysis to elucidate the signaling requirements for embryonic axis and limb development, with a focus on FGF signaling. Understanding how these pathways signal during development often informs us how they signal in various diseases, including cancer. An example of this work is Dr. Anderson’s identification of a novel signaling requirement for Fgf3 to limit BMP signaling in the forming neural tube. When the gene encoding Fgf3 is inactivated, mice develop neural tube and posterior axis defects, because of increased BMP signaling within the dorsal neural tube and axial progenitor tissue. Neural tube defects are exacerbated when BMP signaling is genetically increased, and in some cases leads to spina bifida and spina bifida occulta, a common human congenital malformation.
Areas of Expertise
1) FGF signaling 2) imaging 3) mouse genetics 4) genome manipulation
The focus of my work is understanding the redundant and non-redundant functions of fibroblast growth factors (FGFs) during embryonic development through use of mouse models. FGFs are secreted factors that are important in a number of cellular processes including cell division, survival, migration, and cell fate decisions. An area of specific interest is understanding FGF requirements in the presomitic mesoderm (PSM), the progenitor tissue of the axis. Somites are segmented from the anterior PSM and give rise to the segmented and non-segmented structures of the adult body, including the vertebrae, muscles, and the dermis of the torso. At least 7 Fgf family members are expressed in or around the PSM (Fgf3, Fgf4, Fgf5, Fgf8, Fgf15, Fgf17 and Fgf18). We have previously shown redundant and non-redundant requirements for some of these genes and are currently interested in FGF interactions with Notch signaling components important in somite segmentation. These Notch signaling components change dynamically and tightly interact with each other, prompting us to utilize multiplex fluorescent wholemount mRNA detection to examine the expression of these genes. Coupled with confocal imaging and computer modeling we are able to quantify the expression of multiple genes within a single embryonic tissue while maintaining spatial relationships.
In addition to the axis, we are also studying FGF signaling in the developing kidney, limb, and pelvic girdle through use of loss of function and gain of function mouse genetics and quantitative fluorescent mRNA analysis.
An FGF3-BMP Signaling Axis Regulates Caudal Neural Tube Closure, Neural Crest Specification and Anterior-Posterior Axis Extension
Fgf3-Fgf4-cis: A new mouse line for studying Fgf functions during mouse development
BMPs are direct triggers of interdigital programmed cell death
FGF-Regulated Etv Transcription Factors Control FGF-SHH Feedback Loop in Lung Branching
TCreERT2, a transgenic mouse line for temporal control of Cre-mediated recombination in lineages emerging from the primitive streak or tail bud
Matthew J. Anderson, Ph.D.
Dr. Anderson joined Dr. Mark Lewandoski’s lab in 2008 as a Postdoctoral Fellow, became a Research Fellow in 2013, and then a Staff Scientist in 2016.