Asymmetric cell division during embryogenesis contributes to cell diversity by generating daughter cells that adopt distinct developmental fates. Little is known about how many of these asymmetric divisions are regulated, but two papers in this issue suggest that FGF signalling plus an ectoderm-derived signal control asymmetric division and the specification of notochord/neural precursors in ascidian embryos. In these embryos, two pairs of mother cells give rise to neural and notochord precursors. Daughter cells in which ERK is activated develop into notochord cells, whereas the others develop into neural cells. But FGF and its receptor, which activate ERK, are widely distributed in the mother cells and surrounding vegetal cells, so how is an asymmetric cue generated? On p. 1491,Picco and colleagues show that the segregation of notochord and neural fates in Ciona embryos is an intrinsic property of the mother cells that is acquired through their interaction with ectoderm precursors. This interaction is mediated by the ephrin-Eph signalling system, which is better known for its roles in axon guidance and cell adhesion. The inhibition of ephrin-Eph signalling causes symmetric cell division and generates only notochord precursors, the researchers report. The ephrin-Eph signal attenuates ERK activation in the neural-fated daughter cell. Thus, a directional ephrin-Eph signal from the ectoderm polarises the notochord/neural mother cell and asymmetrically modulates ERK activation and fate specification in the daughter cells. On p. 1509, Kim and colleagues examine the specification of notochord/neural precursors and of mesenchyme/muscle precursors in another ascidian, Halocynthia roretzi. They find that a directional FGF signal alone determines the asymmetric division of the muscle/mesenchyme mother cells, but that an FGF antagonising signal from the neighbouring ectoderm controls the polarity of the notochord/neural mother cells. This signal suppresses FGF signal transduction in the neural-fated daughter cell and the expression of FoxA, which encodes an essential transcription factor for notochord formation. Together, these two papers provide strong evidence for a new mechanism by which FGF signalling, in combination with an antagonising signal from the ectoderm, controls asymmetric cell division and cell fate specification during ascidian notochord/neural development.
Asymmetric cell division: fateful FGF antagonism
Asymmetric cell division: fateful FGF antagonism. Development 15 April 2007; 134 (8): e802. doi:
Download citation file:
Advertisement
Cited by
Pathway to Independence programme

We’re excited to announce our new Pathway to Independence programme, aimed at supporting postdocs as they go on the job market. Find out more about the scheme in our Editorial.
Call for papers: Metabolic and Nutritional Control of Development and Regeneration

We are welcoming submissions for our next special issue, which will focus on metabolic and nutritional control of development and regeneration. Submission deadline: 15 May 2023.
Webinar: Increasing the visibility and impact of your research
-HUBSwebinar.jpg?versionId=4486)
Would you like to increase the visibility and impact of your research and raise your profile internationally? If so, register for the very practical webinar we are running in association with HUBS on 23 February 2023.
Transitions in development: Daniel Grimes

Daniel Grimes’s lab studies the consequences of ciliary mutations, including left-right patterning defects and scoliosis. We interviewed Daniel to find out more about his career path, his experience of becoming a group leader and the influence of Jurassic Park.
Preprints in Development
(update)-InPreprints.png?versionId=4486)
As part of our efforts to support the use of preprints and help curate the preprint literature, we are delighted to launch a new article type: ‘In preprints’. These pieces will discuss one or more recent preprints and place them in a broader context.