Beyond cell proliferation in avian facial morphogenesis

Linde‐Medina, Marta; Hallgrímsson, Benedikt; Marcucio, Ralph

doi:10.1002/dvdy.24374

Cited by 4 publications

(2 citation statements)

References 49 publications

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“…This intricate signaling crosstalk coordinates the convergent growth and morphogenesis of the facial prominences that is essential for aligning these structures prior to fusion (e.g. Geetha-Loganathan et al, 2014; Green et al, 2015; Hu et al, 2015; Linde-Medina et al, 2016; Suzuki et al, 2016). Subsequent interactions between the apposed epithelia then consummate lip and palate fusion (reviewed in Kousa and Schutte, 2016).…”

Section: Introductionmentioning

confidence: 99%

Systems biology of facial development: contributions of ectoderm and mesenchyme

Hooper

Feng

et al. 2017

Developmental Biology

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The rapid increase in gene-centric biological knowledge coupled with analytic approaches for genomewide data integration provides an opportunity to develop systems-level understanding of facial development. Experimental analyses have demonstrated the importance of signaling between the surface ectoderm and the underlying mesenchyme in coordinating facial patterning. However, current transcriptome data from the developing vertebrate face is dominated by the mesenchymal component, and the contributions of the ectoderm are not easily identified. We have generated transcriptome datasets from critical periods of mouse face formation that enable gene expression to be analyzed with respect to time, prominence, and tissue layer. Notably, by separating the ectoderm and mesenchyme we considerably improved the sensitivity compared to data obtained from whole prominences, with more genes detected over a wider dynamic range. From these data we generated a detailed description of ectoderm-specific developmental programs, including pan-ectodermal programs, prominence- specific programs and their temporal dynamics. The genes and pathways represented in these programs provide mechanistic insights into several aspects of ectodermal development. We also used these data to identify co-expression modules specific to facial development. We then used 14 co-expression modules enriched for genes involved in orofacial clefts to make specific mechanistic predictions about genes involved in tongue specification, in nasal process patterning and in jaw development. Our multidimensional gene expression dataset is a unique resource for systems analysis of the developing face; our co-expression modules are a resource for predicting functions of poorly annotated genes, or for predicting roles for genes that have yet to be studied in the context of facial development; and our analytic approaches provide a paradigm for analysis of other complex developmental programs.

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Section: Introductionmentioning

confidence: 99%

Systems biology of facial development: contributions of ectoderm and mesenchyme

Hooper

Feng

et al. 2017

Developmental Biology

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“…Even here, though, patterning of cell proliferation within migrating streams of neural crest cells plays a role (Kulesa et al, 2008). Finally, physical forces influence morphogenesis at multiple levels ranging from interaction with extracellular matrix (Daley and Yamada, 2013;Linde-Medina et al, 2016), among cells due to regulation of cell adhesion (Lecuit, 2005;LeGoff and Lecuit, 2016), and physical interactions between tissues such as the neural tube and facial prominences during morphogenesis (Marcucio et al, 2015;Parsons et al, 2011). These alternative and potentially interacting mechanisms for morphogenesis suggest the need for development of methods to objectively determine the relative contribution of spatiotemporal variation in cell proliferation to fully understand the cellular bases of morphogenesis.…”

Section: Structure Of Growthmentioning

confidence: 99%

Quantifying the relationship between cell proliferation and morphology during development of the face

Green

Vercio

Dauter

et al. 2023

Preprint

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Morphogenesis requires highly coordinated, complex interactions between cellular processes: proliferation, migration, and apoptosis, along with physical tissue interactions. How these cellular and tissue dynamics drive morphogenesis remains elusive. Three dimensional (3D) microscopic imaging poses great promise, and generates beautiful images. However, generating even moderate through-put quantified images is challenging for many reasons. As a result, the association between morphogenesis and cellular processes in 3D developing tissues has not been fully explored. To address this critical gap, we have developed an imaging and image analysis pipeline to enable 3D quantification of cellular dynamics along with 3D morphology for the same individual embryo. Specifically, we focus on how 3D distribution of proliferation relates to morphogenesis during mouse facial development. Our method involves imaging with light-sheet microscopy, automated segmentation of cells and tissues using machine learning-based tools, and quantification of external morphology via geometric morphometrics. Applying this framework, we show that changes in proliferation are tightly correlated to changes in morphology over the course of facial morphogenesis. These analyses illustrate the potential of this pipeline to investigate mechanistic relationships between cellular dynamics and morphogenesis during embryonic development.

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Downstream branches of receptor tyrosine kinase signaling act interdependently to shape the face

Hanne,

Hu,

Vidal-García

et al. 2024

Preprint

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BackgroundPreviously we found that increasing fibroblast growth factor (FGF) signaling in the neural crest cells within the frontonasal process (FNP) of the chicken embryo caused dysmorphology that was correlated with reduced proliferation, disrupted cellular orientation, and lower MAPK activation but no change in PLCy and PI3K activation. This suggests RTK signaling may drive craniofacial morphogenesis through specific downstream effectors that affect cellular activities. In this study we inhibited three downstream branches of RTK signaling to determine their role in regulating cellular activities and how these changes affect morphogenesis of the FNP.ResultsSmall molecule inhibitors of MEK1/2, PI3K, and PLCy were delivered individually and in tandem to the right FNP of chicken embryos. All treatments caused asymmetric proximodistal truncation on the treated side and a mild expansion on the untreated side compared to DMSO control treated FNPs. Inhibiting each pathway caused similar decreased proliferation and disrupted cellular orientation, but did not affect apoptosis.ConclusionsSince RTK signaling is a ubiquitous and tightly regulated biochemical system we conclude that the downstream pathways are robust to developmental perturbation through redundant signaling systems.Bullet pointsInhibiting three downstream effectors of receptor tyrosine kinase (RTK) signaling (MEK1/2, PLCy, and PI3K) in the frontonasal process of chicken embryos caused similar mild truncation of growth. Combining all three inhibitors had a slightly stronger effect on truncation.Individual inhibitors did not have specific effects on cellular proliferation, apoptosis, or cellular orientation.The downstream branches of RTK signaling likely have shared interdependent effects on cellular activities that contribute to morphogenesis.

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Beyond cell proliferation in avian facial morphogenesis

Cited by 4 publications

References 49 publications

Systems biology of facial development: contributions of ectoderm and mesenchyme

Systems biology of facial development: contributions of ectoderm and mesenchyme

Quantifying the relationship between cell proliferation and morphology during development of the face

Downstream branches of receptor tyrosine kinase signaling act interdependently to shape the face

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