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Greaves, S.

Publications and source records attributed to Greaves, S..

2 recordsLinked to original sources

Tetraspanin Cd9b plays a role in fertility in zebrafish

In mice, CD9 expression on the egg is required for efficient sperm-egg fusion and no effects on ovulation or male fertility are observed in CD9 null animals. Here we show that cd9b KO zebrafish also appear to have fertility defects. In contrast to mice, fewer eggs were laid by cd9b KO zebrafish pairs and, of the eggs laid, a lower percentage were fertilised. In vitro fertilization (IVF) was used to demonstrate that factors such as courting behaviour, adult size and mate choice were not causing the unexpected decrease in clutch size. The decrease in egg numbers could be rescued by exchanging either cd9b KO partner, male or female, for a wildtype (WT) partner. However, the fertilisation defect could only be rescued by crossing a cd9b KO female with a WT male. Our results indicate that Cd9b has several roles in fish fertility, affecting both clutch size and egg fertilisation. HighlightsO_LIcd9b mutant pairs lay fewer eggs and of the eggs laid, fewer are fertilised. C_LIO_LIMutation in cd9b does not affect primordial germ cell number or migration. C_LIO_LIReduction in number of eggs and fertility is not due to courting behaviour, fish size or mate choice. C_LIO_LIcd9b mutation in either gender affects the number of eggs laid. C_LIO_LIMutation of cd9b in the males affects fertilisation efficiency but mutation of cd9b in the females does not. C_LI

developmental biology↗

CD9 tetraspanins convey robustness to CXCR4b signalling during collective cell migration

Collective cell migration is essential for embryonic development and homeostatic processes. During zebrafish development, the posterior lateral line primordium (pLLP) navigates along the embryo flank by collective cell migration. The chemokine receptors, Cxcr4b and Cxcr7b, as well as their cognate ligand, Cxcl12a, are essential for this process. We corroborate that knockdown of the zebrafish cd9 tetraspanin orthologue, cd9b, results in mild pLL abnormalities. Through generation of CRISPR and TALEN mutants, we show that cd9a and cd9b function partially redundantly in pLLP migration, which is delayed in the cd9b single and cd9a; cd9b double mutants. This delay led to a transient reduction in neuromast numbers. Loss of both Cd9a and Cd9b sensitized embryos to reduced Cxcr4b and Cxcl12a levels. Together these results provide evidence that Cd9 modulates collective cell migration of the pLLP during zebrafish development. One interpretation of these observations is that Cd9 contributes to more effective chemokine signalling.

developmental biology↗