Mutation of the central nervous system neuroblast proliferation repressorana leads to defects in larval olfactory behavior
✍ Scribed by Park, Youngji ;Caldwell, M. Craig ;Datta, Sumana
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 375 KB
- Volume
- 33
- Category
- Article
- ISSN
- 0022-3034
No coin nor oath required. For personal study only.
✦ Synopsis
In the developing nervous system, sayed in a behavioral paradigm. When tested with interactions between glia and immature neurons or the three different chemoattractants, third instar ana 9 neuroblasts regulate axon pathfinding, migration, and mutant larvae showed diminished olfactory response cell division, and therefore affect structure and funccompared to controls. Examination of a second ana tion. Glial control of neuroblast cell division has been allele revealed aberrant olfactory response to ethyl documented by studies of the anachronism (ana) gene acetate, demonstrating that more than one mutation of Drosophila melanogaster. ana encodes a glycoproin ana can give rise to abnormal larval olfactory betein which, in the developing larval central nervous havior. Assays of early first instar ana 9 mutant larvae system, is secreted by glia that neighbor regulated revealed defective olfactory behavior, implying that neuroblasts. Mutations in ana lead to premature neuthe olfactory phenotype stems from early larval AMC roblast proliferation in the larval brain. Examination and/or embryonic origins. This is consistent with proof lacZ expression from an ana enhancer trap line as liferation analysis in the early larval AMC region well as detection of the ana protein show that ana is which uncovered a significantly higher number of Salso expressed in the larval antennal-maxillary comphase cells in ana 9 mutants. ᭧ 1997 John Wiley & Sons, plex (AMC) at all larval stages. As previously re-