Kenneth Poss

Overview:

Modeling disease in zebrafish
Genetic approaches to organ regeneration
Cardiac regeneration
Appendage regeneration
Developmental biology

Positions:

James B. Duke Distinguished Professor of Cell Biology

Cell Biology
School of Medicine

Professor of Cell Biology

Cell Biology
School of Medicine

Professor in Medicine

Medicine, Cardiology
School of Medicine

Professor of Biology

Biology
Trinity College of Arts & Sciences

Associate of the Duke Initiative for Science & Society

Duke Science & Society
Institutes and Provost's Academic Units

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Director of the Duke Regeneration Center

Regeneration Next Initiative
School of Medicine

Education:

Ph.D. 1998

Massachusetts Institute of Technology

Research Fellow

University of Utah

Postdoctoral Fellow, Cardiology

Children's Hospital

Grants:

Mechanisms protecting cell surface integrity in giant vacuolated cells of the notochord

Administered By
Basic Science Departments
Awarded By
National Institutes of Health
Role
Co-Sponsor
Start Date
End Date

Regulation of the Epicardial Injury Response During Heart Regeneration in Zebrafish

Administered By
Basic Science Departments
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Eliciting heart regeneration through cardiomyocyte division

Administered By
Basic Science Departments
Awarded By
Fondation Leducq
Role
Principal Investigator
Start Date
End Date

Polyploidy in Cardiac Development and Tissue Repair in Drosophila

Administered By
Pharmacology & Cancer Biology
Awarded By
National Institutes of Health
Role
Co-Sponsor
Start Date
End Date

Regulation of Myocardial Regeneration in Zebrafish

Administered By
Basic Science Departments
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Publications:

Deciphering Heart Regeneration by Histone Exchange Profiling.

Authors
Goldman, JA; Kuzu, G; Lee, N; Karasik, J; Gemberling, M; Karra, R; Dickson, A; Tolstorukov, MY; Poss, KD
MLA Citation
Goldman, J. A., et al. “Deciphering Heart Regeneration by Histone Exchange Profiling.Molecular Biology of the Cell, vol. 28, AMER SOC CELL BIOLOGY, 2017.
URI
https://scholars.duke.edu/individual/pub1308362
Source
wos
Published In
Molecular Biology of the Cell
Volume
28
Published Date

NF-kappa B Activity is Required for Heart Regeneration

Authors
Karra, R; Knecht, A; Poss, KD
MLA Citation
Karra, Ravi, et al. “NF-kappa B Activity is Required for Heart Regeneration.” Circulation, vol. 130, LIPPINCOTT WILLIAMS & WILKINS, 2014.
URI
https://scholars.duke.edu/individual/pub1328042
Source
wos
Published In
Circulation
Volume
130
Published Date

Mathematical modeling of Erk activity waves in regenerating zebrafish scales.

Erk signaling regulates cellular decisions in many biological contexts. Recently, we have reported a series of Erk activity traveling waves that coordinate regeneration of osteoblast tissue in zebrafish scales. These waves originate from a central source region, propagate as expanding rings, and impart cell growth, thus controlling tissue morphogenesis. Here, we present a minimal reaction-diffusion model for Erk activity waves. The model considers three components: Erk, a diffusible Erk activator, and an Erk inhibitor. Erk stimulates both its activator and inhibitor, forming a positive and negative feedback loop, respectively. Our model shows that this system can be excitable and propagate Erk activity waves. Waves originate from a pulsatile source that is modeled by adding a localized basal production of the activator, which turns the source region from an excitable to an oscillatory state. As Erk activity periodically rises in the source, it can trigger an excitable wave that travels across the entire tissue. Analysis of the model finds that positive feedback controls the properties of the traveling wavefront and that negative feedback controls the duration of Erk activity peak and the period of Erk activity waves. The geometrical properties of the waves facilitate constraints on the effective diffusivity of the activator, indicating that waves are an efficient mechanism to transfer growth factor signaling rapidly across a large tissue.
Authors
Hayden, LD; Poss, KD; De Simone, A; Di Talia, S
MLA Citation
Hayden, Luke D., et al. “Mathematical modeling of Erk activity waves in regenerating zebrafish scales.Biophys J, vol. 120, no. 19, Oct. 2021, pp. 4287–97. Pubmed, doi:10.1016/j.bpj.2021.05.004.
URI
https://scholars.duke.edu/individual/pub1483492
PMID
34022234
Source
pubmed
Published In
Biophysical Journal
Volume
120
Published Date
Start Page
4287
End Page
4297
DOI
10.1016/j.bpj.2021.05.004

Transgenic mice for in vivo epigenome editing with CRISPR-based systems.

CRISPR-Cas9 technologies have dramatically increased the ease of targeting DNA sequences in the genomes of living systems. The fusion of chromatin-modifying domains to nuclease-deactivated Cas9 (dCas9) has enabled targeted epigenome editing in both cultured cells and animal models. However, delivering large dCas9 fusion proteins to target cells and tissues is an obstacle to the widespread adoption of these tools for in vivo studies. Here, we describe the generation and characterization of two conditional transgenic mouse lines for epigenome editing, Rosa26:LSL-dCas9-p300 for gene activation and Rosa26:LSL-dCas9-KRAB for gene repression. By targeting the guide RNAs to transcriptional start sites or distal enhancer elements, we demonstrate regulation of target genes and corresponding changes to epigenetic states and downstream phenotypes in the brain and liver in vivo, and in T cells and fibroblasts ex vivo. These mouse lines are convenient and valuable tools for facile, temporally controlled, and tissue-restricted epigenome editing and manipulation of gene expression in vivo.
Authors
Gemberling, MP; Siklenka, K; Rodriguez, E; Tonn-Eisinger, KR; Barrera, A; Liu, F; Kantor, A; Li, L; Cigliola, V; Hazlett, MF; Williams, CA; Bartelt, LC; Madigan, VJ; Bodle, JC; Daniels, H; Rouse, DC; Hilton, IB; Asokan, A; Ciofani, M; Poss, KD; Reddy, TE; West, AE; Gersbach, CA
MLA Citation
Gemberling, Matthew P., et al. “Transgenic mice for in vivo epigenome editing with CRISPR-based systems.Nat Methods, vol. 18, no. 8, Aug. 2021, pp. 965–74. Pubmed, doi:10.1038/s41592-021-01207-2.
URI
https://scholars.duke.edu/individual/pub1492755
PMID
34341582
Source
pubmed
Published In
Nat Methods
Volume
18
Published Date
Start Page
965
End Page
974
DOI
10.1038/s41592-021-01207-2

The RNA helicase Ddx52 functions as a growth switch in juvenile zebrafish.

Vertebrate animals usually display robust growth trajectories during juvenile stages, and reversible suspension of this growth momentum by a single genetic determinant has not been reported. Here, we report a single genetic factor that is essential for juvenile growth in zebrafish. Using a forward genetic screen, we recovered a temperature-sensitive allele, pan (after Peter Pan), that suspends whole-organism growth at juvenile stages. Remarkably, even after growth is halted for a full 8-week period, pan mutants are able to resume a robust growth trajectory after release from the restrictive temperature, eventually growing into fertile adults without apparent adverse phenotypes. Positional cloning and complementation assays revealed that pan encodes a probable ATP-Dependent RNA Helicase (DEAD-Box Helicase 52; ddx52) that maintains the level of 47S precursor ribosomal RNA. Furthermore, genetic silencing of ddx52 and pharmacological inhibition of bulk RNA transcription similarly suspend the growth of flies, zebrafish and mice. Our findings reveal evidence that safe, reversible pauses of juvenile growth can be mediated by targeting the activity of a single gene, and that its pausing mechanism has high evolutionary conservation.
Authors
Tseng, T-L; Wang, Y-T; Tsao, C-Y; Ke, Y-T; Lee, Y-C; Hsu, H-J; Poss, KD; Chen, C-H
MLA Citation
Tseng, Tzu-Lun, et al. “The RNA helicase Ddx52 functions as a growth switch in juvenile zebrafish.Development, July 2021. Pubmed, doi:10.1242/dev.199578.
URI
https://scholars.duke.edu/individual/pub1487521
PMID
34224557
Source
pubmed
Published In
Development
Published Date
DOI
10.1242/dev.199578