GSBS Student Publications

Title

Roles of Drosophila Kruppel-homolog 1 in neuronal morphogenesis

Student Author(s)

Lei Shi; Suewei Lin

GSBS Program

Neuroscience

UMMS Affiliation

Department of Neurobiology; Tzumin Lee Lab; Graduate School of Biomedical Sciences, Neuroscience Program

Date

10-2007

Document Type

Article

Medical Subject Headings

Animals; Body Patterning; Brain; Drosophila; Drosophila Proteins; Ecdysone; *Gene Expression Regulation, Developmental; Immunohistochemistry; Kruppel-Like Transcription Factors; Larva; Metamorphosis, Biological; Microscopy, Confocal; Morphogenesis; Mosaicism; Mushroom Bodies; Neurons; Pupa

Disciplines

Neuroscience and Neurobiology

Abstract

The molecular mechanisms underlying remodeling of neural networks remain largely unknown. In Drosophila, widespread neural remodeling occurs during metamorphosis, and is regulated by ecdysone. Kruppel-homolog 1 (Kr-h1) is a zinc finger transcription factor known to play a role in orchestrating ecdysone-regulated transcriptional pathways and, furthermore, implicated in governing axon morphogenesis. Interestingly, in honey bee workers, neural expression of the Apis mellifera homolog of Kr-h1 is enhanced during their transition to foraging behavior when there is increased neurite outgrowth, branching, and synapse formation. Here, we assessed the role(s) of KR-H1 in Drosophila neuronal remodeling and morphology. We characterized the effect of Kr-h1 expression on neuronal morphology through Drosophila larval, pupal, and adult stages. Increased expression of Kr-h1 led to reduced branching in individual neurons and gross morphological changes in the mushroom bodies (MBs), while knocking down Kr-h1 did not produce any obvious changes in neural morphology. Drosophila Kr-h1 is normally expressed when MB neurons do not undergo active morphogenesis, suggesting that it may play a role in inhibiting morphogenesis. Further, loss of endogenous KR-H1 enhanced the neuronal morphogenesis that is otherwise delayed due to defective TGF-beta signaling. However, loss of KR-H1 alone did not affect neuronal morphogenesis. In addition, Kr-h1 expression remains strongly linked to ecdysone-regulated pathways: Kr-h1 expression is regulated by usp, which dimerizes to the ecdysone receptor, and Kr-h1 expression is essential for proper patterning of the ecdysone receptor isoforms in the late larval central nervous system. Thus, although KR-H1 has a potential for modulating neuronal morphogenesis, it appears physiologically involved in coordinating general ecdysone signaling.

Rights and Permissions

Citation: Dev Neurobiol. 2007 Oct;67(12):1614-26. Link to article on publisher's site

DOI of Published Version

10.1002/dneu.20537

Related Resources

Link to Article in PubMed

Journal Title

Developmental neurobiology

PubMed ID

17562531