High impact information on loco

• Locomotion defects, together with Pins, regulates heterotrimeric G-protein signaling during Drosophila neuroblast asymmetric divisions [1].
• This suggests that loco and pros are targets of DRI transcriptional activation in some LG [2].
• However, from stage 15 of embryogenesis, expression of locomotion defects (loco) and prospero (pros) was found to be missing in a subset of LG [2].
• Ultrastructural analysis of homozygous mutant loco embryos reveals a severe glial cell differentiation defect [3].
• Hypomorphic loco alleles were isolated following an EMS mutagenesis [3].

Biological context of loco

• Using an enhancer trap approach, we have identified loco as such a gene. loco is expressed in most lateral CNS glial cells throughout development [3].
• During subsequent stages of embryonic development gcm and pointed appear to activate loco transcription synergistically [4].
• Using promoter-reporter gene fusions we identified a 1.9 kb promoter element capable of directing the almost complete loco gene expression pattern [4].
• At least two transcripts of loco are expressed in oogenesis, loco-c2 is observed in the anterior-dorsal follicle cells and is downstream of the epidermal growth factor receptor signalling pathway, initiated in the oocyte. loco-c3 is a new transcript of loco, which is expressed in the nurse cells from stage 6 onwards [5].

Anatomical context of loco

• In addition, at least two other factors appear to repress loco expression in the ectoderm and in the CNS midline cells [4].
• Analysis of newly generated mutants and antisense technology enabled us to establish that disrupting loco in follicle cells results in ventralized eggs, while disrupting loco in nurse cells results in short eggs, due to defective dumping of the nurse cell cytoplasm into the oocyte [5].

Other interactions of loco

• The expression of loco is initially dependent on gcm [4].

References