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A more recent version of this article appeared on October 1, 2005
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Submitted on March 14, 2005
Revised on July 12, 2005
Accepted on July 14, 2005
*Department of Molecular, Cellular, and Developmental Biology and Howard Hughes Medical Institute and
Boulder Laboratory for 3-D Electron Microscopy of Cells, University of Colorado-Boulder, Boulder, CO 80303
Monitoring Editor: Jean Schwarzbauer
The homeobox-containing aristaless-related protein, ARX, has been directly linked to the development of a number of human disorders involving mental retardation and epilepsy and clearly plays a critical role in development of the vertebrate CNS. In this work, we investigate the role of ALR-1,the C. elegans aristaless orthologue, in amphid sensory function. Our studies indicate that ALR-1is required for maintenance of the amphid organ structure throughout larval development. Mutant analysis indicates a progressive loss in the amphid neurons ability to fill with lypophilic dyes as well as a declining chemotactic response. The degeneration in amphid function corresponds with a failure of the glial-like amphid socket cell to maintain its specific cell shape and cell-cell contacts. Consistent with ALR-1 expression within the amphid socket cell, our results indicate a cell autonomous role for ALR-1 in maintaining cell shape. Furthermore, we demonstrate a role for ALR-1 in the proper morphogenesis of the anterior hypodermis. Genetic interaction tests also suggest that ALR-1may function cooperatively with the cell adhesion processes in maintaining the amphid sensory organs.
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