bendless, a Drosophila gene affecting neuronal connectivity, encodes a ubiquitin-conjugating enzyme homolog
The Drosophila bendless (ben) gene was originally isolated as a mutation affecting the escape jump response. This behavioral defect was ascribed to a single lesion affecting the connectivity between the giant fiber and the tergotrochanter motor neuron. A closer examination of the ben phenotype suggests that ben activity is broader and affects a variety of other neurons including photoreceptor cells and their axons. Mosaic analysis indicates that the focus of ben activity is presynaptic. We have cloned the ben gene through a chromosomal walk and show that it is homologous to a class of ubiquitin-conjugating enzymes. The major role of ubiquitination in the protein degradative pathway suggests that ben regulates neural developmental processes such as growth cone guidance by targeting specific proteins for degradation.
© 1994 Society for Neuroscience. Beginning six months after publication the Work will be made freely available to the public on SfN's website to copy, distribute, or display under a Creative Commons Attribution 4.0 International (CC BY 4.0) license (https://creativecommons.org/licenses/by/4.0/). Received June 24, 1993; revised Oct. 22, 1993; accepted Nov. 1, 1993. We thank Drs. William Trevarrow and Ken McCormack for contributions to asnects of this work. We are grateful for technical assistance from Rommel Valero. Kawanaa Areceneaux, and Rosalind Young, and the management of fly stocks by Sally Faulhaber. We thank Drs. Mani Ramaswami, Elaine Reynolds, Jeremy Lee, and Paul Pavlidis for critical reading of the manuscript. This research was supported by a fellowship from the Jane Coffin Childs Memorial Fund for Medical Research and an NIH postdoctoral fellowship to C.E.O., NSF Grant BNS 9120084 to M.A.T., and grants to S.B. from the NSF (BCS8908154) the NIH (EY09278), and the James G. Boswell Foundation. During the review of this manuscript, an article by Muralidhar and Thomas (1993) was published that also describes the cloning of the ben gene. They cite our earlier unpublished findings that ben^1 has neuronal defects additional to the GF defect and confirm many others of our observations. In addition, their experiments with ben-bithorax mutants provide support for the models we have presented.
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