Expression of an extracellular deletion of Xotch diverts cell fate in Xenopus embryos
Article Abstract:
A study of the role of Xotch in cell fate determination in Xenopus embryos is presented. Xotch is the Xenopus homolog of Notch, a receptor involved in cell fate determination in Drosophila. The study involved the expression of an extracellular deletion construct of Xotch called Xotch-Delta-E in Xenopus embryos. The results showed that Xotch-Delta-E causes consistent histogenic defects such as loss or hypertrophy of certain tissues, and extends the normal time course over which tissues are responsive to inductive signals. The results suggest that Xotch-Delta-E delays differentiation and diverts the course of differentiation.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1993
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Attraction versus repulsion: modular receptors make the difference in axon guidance
Article Abstract:
A study was conducted to identify the molecular mechanism that guide axons along their stereotypical pathways and to determine how axons respond to bifunctional guidance cues. Experiments with the Xenopus axon turning assay revealed that transmembrane receptors determine whether the growth cone along the axons' pathway see guidance cues as attractive or repulsive. It was also found that heteromeric receptors control the response of growth cones to bifunctional guidance cues.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1999
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Giant eyes in Xenopus laevis by overexpression of XOptx2
Article Abstract:
The Xenopus Optx2 homolog (XOptx2) was isolate, characterized and overexpressed to investigate its role in the regulation of vertebrate eye size. The overexpression of XOptx2 resulted to a dramatic increase eye size. Retionblasts transfected with XOptx2 were found to produce clones of cells that are about twice as large as control clones. Results also showed that Pax6 cannot increase eye size alone, but acts synergistically with XOptx2.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1999
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