Author

Michael M. Scott

University of Virginia

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Developmental Biology· 2 Neuroscience· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Amelie Kuchler· 1 shared Anusha U. Saga· 1 shared Casey D. GaileyiD· 1 shared Daniel M. Warthen· 1 shared David L. BrautiganiD· 1 shared Eric J. Wang· 1 shared Eric R. WengertiD· 1 shared Jessica E. BiddingeriD· 1 shared

Activity by Year

2020-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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1 shared paperNeuroscience

Amelie Kuchler

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

DNA Methyltransferase 1 and 3a Expression in the Frontal Cortex Regulates Palatable Food Consumption

Mohan C. Manjegowda, Jonathan Joy-Gaba, Eric R. Wengert, Anusha U. Saga, Daniel M. Warthen, Amelie Kuchler, Ronald Petrus Albertus Gaykema, Manoj K. Patel, Nathan C. Sheffield, Michael M. Scott

This study shows that deleting DNA methyltransferase 1 and 3a in the mouse prefrontal cortex reduces palatable food consumption without affecting chow intake, with effects on neuron excitability and DNA methylation patterns.

bioRxiv · May 23, 2021 · PreprintNeuroscience

Leptin suppresses development of GLP-1 Inputs to the Paraventricular Nucleus of the Hypothalamus

Jessica E. Biddinger, Roman M. Lazarenko, Michael M. Scott, Richard B. Simerly

This study shows that leptin reduces excitatory input from PPG neurons to PVH GLP-1 receptor neurons, diminishing visceral sensory impact on these neurons.

eLife · Nov 18, 2020Peer-reviewedDevelopmental Biology

Phosphosite T674A mutation in kinesin family member 3A fails to reproduce tissue and ciliary defects characteristic of CILK1 loss of function

Casey D. Gailey, Eric J. Wang, Li Jin, Sean Ahmadi, David L. Brautigan, Xudong Joshua Li, Wenhao Xu, Michael M. Scott, Zheng Fu

The paper shows that mutating KIF3A's phosphorylation site T674 to Ala in mice does not reproduce the severe ciliopathy defects seen with CILK1 loss of function.

Developmental Dynamics · Sep 16, 2020Peer-reviewedDevelopmental Biology