Projects per year
Abstract
The Golgi is essential for glycosylation of newly synthesised proteins including almost all cell-surface and extracellular matrix proteoglycans. Giantin, encoded by the golgb1 gene, is a member of the golgin family of proteins that reside within the Golgi stack but its function remains elusive. Loss-of-function of giantin in rats causes osteochondrodysplasia; knockout mice show milder defects, notably a cleft palate. In vitro, giantin has been implicated in Golgi organisation, biosynthetic trafficking, and ciliogenesis. Here we show that loss-of-function of giantin in zebrafish, using either morpholino or knockout techniques, causes defects in cilia function. Giantin morphants have fewer cilia in the neural tube and those remaining are longer. Mutants have the same number of cilia in the neural tube but these cilia are also elongated. Scanning electron microscopy shows that loss of giantin results in an accumulation of material at the ciliary tip, consistent with a loss-of-function of retrograde intraflagellar transport. Mutants show milder defects than morphants consistent with adaptation to loss of giantin.
Original language | English |
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Pages (from-to) | 1180-1189 |
Number of pages | 10 |
Journal | Biology Open |
Volume | 6 |
Issue number | 8 |
Early online date | 25 May 2017 |
DOIs | |
Publication status | Published - 15 Aug 2017 |
Keywords
- Golgi
- Golgi matrix
- cilia
- zebrafish
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Dive into the research topics of 'The Golgi matrix protein giantin is required for normal cilia function in zebrafish'. Together they form a unique fingerprint.Projects
- 2 Finished
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A dual role for the Golgi matrix protein giantin in extracellular matrix secretion and cilia function
Bergen, D. J. M., Stephens, D. J. & Hammond, C. L.
1/10/12 → 14/11/17
Project: Research
Equipment
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Wolfson Bioimaging Facility
Mark Jepson (Manager)
Faculty of Life SciencesFacility/equipment: Facility