EB1 Is Essential during Drosophila Development and Plays a Crucial Role in the Integrity of Chordotonal Mechanosensory OrgansV⃞
AUTOR(ES)
Elliott, Sarah L.
FONTE
The American Society for Cell Biology
RESUMO
EB1 is a conserved microtubule plus end tracking protein considered to play crucial roles in microtubule organization and the interaction of microtubules with the cell cortex. Despite intense studies carried out in yeast and cultured cells, the role of EB1 in multicellular systems remains to be elucidated. Here, we describe the first genetic study of EB1 in developing animals. We show that one of the multiple Drosophila EB1 homologues, DmEB1, is ubiquitously expressed and has essential functions during development. Hypomorphic DmEB1 mutants show neuromuscular defects, including flightlessness and uncoordinated movement, without any general cell division defects. These defects can be partly explained by the malfunction of the chordotonal mechanosensory organs. In fact, electrophysiological measurements indicated that the auditory chordotonal organs show a reduced response to sound stimuli. The internal organization of the chordotonal organs also is affected in the mutant. Consistently, DmEB1 is enriched in those regions important for the structure and function of the organs. Therefore, DmEB1 plays a crucial role in the functional and structural integrity of the chordotonal mechanosensory organs in Drosophila.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=545920Documentos Relacionados
- Dictyostelium EB1 Is a Genuine Centrosomal Component Required for Proper Spindle FormationV⃞
- EB1–Microtubule Interactions in Xenopus Egg Extracts: Role of EB1 in Microtubule Stabilization and Mechanisms of Targeting to Microtubules
- γ-Tubulin Plays an Essential Role in the Coordination of Mitotic EventsV⃞
- Transcriptional interference between the EBV transcription factors EB1 and R: both DNA-binding and activation domains of EB1 are required.
- Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance