Cell Fate Determination at the Insect CNS Midline

Author: Kung, Te-Yi

Year: 1998

Degree: Dissertation (Ph.D.)

Advisor: Zinn, Kai George

Committee Members: Zinn, Kai George; Anderson, David J.; Kennedy, Mary B.; Lipshitz, Howard D.; Sternberg, Paul W.

Option: Neurobiology

DOI: 10.7907/nm2j-6166

Abstract

The central nervous system (CNS) of insect embryos develops from a neuroepithelial sheet that is patterned by the activities of segmentation genes. Neuroblasts delaminate from this sheet and divide once to produce two ganglion mother cells (GMCs). There are ~ 30 lateral neuroblasts arranged in a regular array in each thoracic and abdominal segment. The GMC progeny differentiate and give rise to neurons and glial cells. These are born in specific positions, and the neurons extend axons along stereotyped trajectories.

Our group has always been interested in the cellular and molecular mechanisms involved in the formation and maintenance of the CNS cell fate map.

In the second chapter of this thesis, I report the isolation and characterization of a cDNA clone encoding a novel Drosophila nonreceptor protein tyrosine phosphatase (PTP), denoted DPTP61F. DPTP61F is closely related to the mammalian PTP1B and the T cell PTP. We show that DPTP61F mRNA is selectively expressed in a pattern of 15 segmental stripes in germband extended embryos. This expression pattern is characteristic of zygotic segment polarity genes, and suggests that DPTP61F activity may be involved in the process of segmental determination. Later in development, DPTP61F is expressed in the CNS.

In Chapters III and IV, I focus on the embryonic development of the CNS midline. In Chapter III, I describe the cloning of the grasshopper singk-minded (Gsim) gene, and the characterization of its expression patterns as well as its putative functions as the master regulator of midline genes.

In Chapter IV, I describe the roles of the cAMP-dependent protein kinase (PKA) in the development of the Drosophila CNS midline. We find that ectopic expression of PK.A in the midline increases the number of BarH1-expressing midline neurons. We also show that local inhibition of PKA in the developing midline results in the death of midline glia during late embryo genesis. The loss of the glia apparently cause CNS axons to follow abnormal pathways.

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