Notch and Cdk5 in Zebrafish <i>mindbomb</i> Mutant: Co-regulation or Coincidence?

Kanungo, Jyotshna; Goswami, M. T.; Pant, H. C.

doi:10.14712/fb2018064020035

Folia Biologica > Archive > 2018, Vol. 64 > Issue 2 > Notch and Cdk5 in Zebrafish…

Fol. Biol. 2018, 64, 35-40

https://doi.org/10.14712/fb2018064020035

Notch and Cdk5 in Zebrafish mindbomb Mutant: Co-regulation or Coincidence?

Jyotshna Kanungo^1,2, M. T. Goswami³, H. C. Pant²

¹Division of Neurotoxicology, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR, USA
²National Institute of Neuronal Disorders and Stroke, National Institute of Health, Bethesda, MD, USA
³National Institute of Children’s Health and Development, National Institute of Health, Bethesda, MD, USA

Received May 2018
Accepted May 2018

Notch signalling is critical for the development of the nervous system. In the zebrafish mindbomb mutants, disruption of E3 ubiquitin ligase activity inhibits Notch signalling. In these mutant embryos, precocious development of primary neurons leading to depletion of neural progenitor cells results in a neurogenic phenotype characterized by defects in neural patterning and brain development. Cyclin-dependent kinase 5 (Cdk5), a predominant neuronal kinase, is involved in a variety of essential functions of the nervous system. Most recently, mammalian studies on Notch and Cdk5 regulating each other’s function have been emerging. The status of Cdk5 in the mindbomb mutant embryos with excessive primary neurons is not known. In situ hybridization of the zebrafish mindbomb mutant embryos uncovered a robust upregulation in Cdk5 expression but with a reduced Cdk5 activity. The implications of these findings in both the mammalian system and zebrafish are discussed in this mini-review to provide a glimpse into the relationship between Notch and Cdk5 that may explain certain neurodevelopmental defects associated with either mutations in ubiquitin ligase or altered expression of Cdk5.