Anthony Fischer, Ph.D.

Postdoctoral Research Associate, Washington University in St. Louis

Anthony Fischer is a skilled and dedicated researcher in the field of molecular biology. He graduated from the University of Missouri-St. Louis (UMSL) in 2018 with a degree in biology, where he developed a strong interest in post-transcriptional gene regulation.
During his time at UMSL, he conducted research on the regulation of mRNA decay through the binding of Pumilio proteins to the 3’UTR region of mRNA molecules, and the implications this had on nutrient sensing and ribosome synthesis. This work involved a combination of experimental techniques, including protein-protein interaction assays, RNA quantification, cell culture and fluorescence microscopy.

After graduation he briefly began postdoctoral research on molecular mechanisms of colorectal cancer before transitioning into studying autism-associated de novo non-coding variants. His current work seeks to adapt current massively parallel reporter assay (MPRA) technology to delineate at which part in an mRNA’s lifecycle the variants are exerting their influence.
Beyond his own research, he is committed to sharing his knowledge and expertise with others. He has mentored several undergraduate and graduate students since the start of his science career, helping them to develop their research skills and contributing to the next generation of scientists.

Principal Investigator: Joseph Dougherty

Fellows: Lily Meyer & Yvette Sol

Undergraduate Fellow Project:

Non-coding mutations are an under-researched area in disease presentation and progression. The non-coding areas of brain-derived messenger RNA (mRNA) are critical for translation initiation, mRNA lifespan and even localization in neurons. Recently, clinicians at our institution have identified 3’ untranslated region (UTR) mutations in a patient family with neurodevelopmental disorder (NDD) that alter mRNA expression profiles and segregate well with the NDD phenotype. Specifically, two affected sons and a maternal uncle all carry the mutation and express the phenotype, while the mother is an unaffected carrier. This suggests the allele interacts with sex to produce the phenotype. The goal of this study is to determine the mechanism of action of this expression difference, validate these findings with protein expression assays, and test whether this effect interacts with sex.

This opportunity will give the SURFiN fellow an opportunity to think critically about all aspects of study. Work done in a research lab can feel disconnected at times for undergraduates if they are not actively involved in every step. The fellow will be involved at each step, including review of the literature, review of initial data, aspects that need further investigation/mechanisms to be uncovered, experimental design with proper controls, data analysis and presentation of findings.

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