Ahmed Mahmoud

Junsu Kang

Assistant Professor
 
PhD, Seoul National University

Postdoctoral Research: Duke University (with Kenneth Poss)

Contact Information
Email: junsu.kang@wisc.edu
4451 WIMR II
1111 Highland Avenue
Madison, WI 53705


Research Interests

We ordinary human beings poorly regenerate most lost tissues including brain, limb and heart. Why do we have limited regenerative capacity and how can we improve this limit? In nature, regenerative capacity varies across species and thus we can get clues from studying a superhero-like animal. Like superheroes, zebrafish spectacularly regenerate almost all damaged tissues or organs including brain, fin and heart, making them an attractive system to study fundamental mechanisms underlying tissue regeneration. In addition, zebrafish is a unique vertebrate model amenable to high-throughput drug screening and forward genetic screening, which cannot be done easily in other vertebrate models. Our laboratory uses zebrafish as a model organism to investigate genetic and epigenetic factors controlling tissue regeneration.

1. Heart regeneration
Most human genes are highly conserved in zebrafish. However, unlike adult humans, zebrafish can regenerate their damaged heart tissues. This discrepancy in heart regeneration is attributable to differential expression of essential genes upon cardiac injury. Major efforts have been made to generate the molecular blueprint of heart regeneration, yet regulatory events are poorly understood. Previously, we reported the first Tissue Regeneration Enhancer Elements (TREEs), short DNA sequences which can activate tissue regeneration programs (Fig. 1). The activity of TREE is very specific: restricted to wound tissues and only during regeneration (Fig. 1). Intriguingly, the specificity of TREE can be engineered with regenerative factor, and we showed that TREE-engineered pro- or anti-regenerative factors do not influence development but are strongly induced upon injury, suggesting that enhancer engineering with TREE can modulate tissue regeneration positively or negatively. Our laboratory will employ various methodologies including transgenic assays, small molecule screening, and biochemical analysis to uncover how cardiac TREE activity is precisely controlled. Investigation of cardiac TREE will allow us to solve the mystery of heart regeneration and further to inspire the therapeutic strategy to unlock our bodies’ latent healing power to give back healthy cardiac tissues to patients.

2. Fin regeneration
Zebrafish is amenable to forward genetic screening, a powerful approach to discover novel factors affecting the phenotype. To identify novel regeneration factors, during my postdoctoral training I carried out forward genetic screening and isolated many mutant families which exhibit fin regeneration defects in a temperature-dependent manner (Fig. 2). We continue to study these mutant families here at UW-Madison. The goal of this project is to identify novel genes and their cellular and molecular mechanisms in fin regeneration and further to determine their roles in regeneration of other tissues including heart. This work will discover novel findings that are important for tissue regeneration.


Representative Publications

  • Kang, J., Hu, J., Karra, R., Dickson, A.L, Tornini, V.A., Nachtrab, G., Gemberling, M., Goldman, J.A., Black, B.L., Poss, K.D. Modulation of tissue repair by regeneration enhancer elements. Nature. 523(7598):201-206, (2016)

  • Kang, J., Karra, R., and Poss, K.D. Back in Black. Developmental Cell. 33(6):623-624, (2015)

  • Kang, J., Nachtrab, G., Poss, K.D., Local Dkk1 Crosstalk from Breeding Ornaments Impedes Regeneration of Injured Male Zebrafish Fins. Developmental  Cell.  27(1):19-31,  (2013)  (This paper is chosen by cover story.)

  • Kang, J.*, Bai, Z.*, Zegarek, M.H., Grant, B.D., Lee, J. Essential roles of snap-29 in C. elegans. Developmental Biology. 355(1):77-88, (2011). (* These two equally contributed to this work)

  • Choi, B., Kang, J., Park, YS., Lee, J., Cho, NJ. A possible role for FRM-1, a C. elegans FERM family protein, in embryonic development. Molecules and Cells. 31(5):455-459, (2011).