Models for patterning primary embryonic body axes: The role of space and time

Meinhardt, Hans

doi:10.1016/j.semcdb.2015.06.005

Cited by 15 publications

(17 citation statements)

References 108 publications

(123 reference statements)

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“…Of two nodal-related genes in zebrafish, Squint (Sqt) functions directly at a distance (Chen & Schier, 2001). Furthermore Sqt induces its inhibitor, Lefty1, which forms a gradient over a greater distance than the activator Nodal, as shown using GFP- or Dendra-tagged proteins, thereby forming a classic reaction-diffusion system (Meinhardt, 2009, 2015; Muller et al, 2012). Attempts to visualize the Nodal gradient have also used reporters such as Smad2:Venus as well as bimolecular fluorescence complementation to visualize the complex between Smad2 and Smad4 (Harvey & Smith, 2009).…”

Section: Other Boundaries and Other Morphogensmentioning

confidence: 99%

“…Recent studies have revealed unexpected dynamics of both ligand and response, positive and negative feedback, and mechanisms for scaling gradients to adjust for changes in tissue size and shape (Fig. 1C,D) (Ben-Zvi, Shilo, & Barkai, 2011; Briscoe & Small, 2015; Horinaka & Morishita, 2012; Meinhardt, 2015). Gene regulatory networks that specify different cell fates based on concentration may elicit different responses depending on regulatory mechanisms (eg, feedback) within the network (Horinaka & Morishita, 2012).…”

Section: Challenges For Morphogen Gradient Studiesmentioning

confidence: 99%

“…Morphogen gradients typically include local sources of ligand production and tightly regulated ligand degradation (Briscoe & Small, 2015; Lander, 2007; Meinhardt, 2015). For RA and A–P patterning of the hindbrain, this arrangement occurs during gastrulation.…”

Section: Feedback Allows Retinoic Acid To Act As a Graded Morphogenmentioning

confidence: 99%

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Visualizing retinoic acid morphogen gradients

Schilling

Sosnik

Nie

2016

Methods in Cell Biology

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Morphogens were originally defined as secreted signaling molecules that diffuse from local sources to form concentration gradients, which specify multiple cell fates. More recently morphogen gradients have been shown to incorporate a range of mechanisms including short-range signal activation, transcriptional/translational feedback, and temporal windows of target gene induction. Many critical cell–cell signals implicated in both embryonic development and disease, such as Wnt, fibroblast growth factor (Fgf), hedgehog (Hh), transforming growth factor beta (TGFb), and retinoic acid (RA), are thought to act as morphogens, but key information on signal propagation and ligand distribution has been lacking for most. The zebrafish provides unique advantages for genetics and imaging to address gradients during early embryonic stages when morphogens help establish major body axes. This has been particularly informative for RA, where RA response elements (RAREs) driving fluorescent reporters as well as Fluorescence Resonance Energy Transfer (FRET) reporters of receptor binding have provided evidence for gradients, as well as regulatory mechanisms that attenuate noise and enhance gradient robustness in vivo. Here we summarize available tools in zebrafish and discuss their utility for studying dynamic regulation of RA morphogen gradients, through combined experimental and computational approaches.

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Section: Other Boundaries and Other Morphogensmentioning

confidence: 99%

Section: Challenges For Morphogen Gradient Studiesmentioning

confidence: 99%

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Visualizing retinoic acid morphogen gradients

Schilling

Sosnik

Nie

2016

Methods in Cell Biology

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“…Kidney development also depends on Fgf 7/10 ligands signaling mostly via the Fgfr1 receptor (Bates, 2007; Rossini et al, 2005), but also Fgfr2 (McMahon, 2016). BMP4 downregulation combined with Fgf expression is an essential early step in neural induction (Fritzsch et al, 2006a; Meinhardt, 2015) that results in an unclear proportion of BMP4/Fgf signaling (Singh and Groves, 2016). This essential step of Bmp4 suppression and Fgf expression is not only essential for placode induction but also suffices to induce stem cells into differentiation as ear organoids in culture (Liu et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Gene, cell, and organ multiplication drives inner ear evolution

Fritzsch

Elliott

2017

Developmental Biology

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We review the development and evolution of the ear neurosensory cells, the aggregation of neurosensory cells into an otic placode, the evolution of novel neurosensory structures dedicated to hearing and the evolution of novel nuclei and their input dedicated to processing those novel auditory stimuli. The evolution of the apparently novel auditory system lies in duplication and diversification of cell fate transcription regulation that allows variation at the cellular level [transforming a single neurosensory cell into a sensory cell connected to its targets by a sensory neuron as well as diversifying hair cells], organ level [duplication of organ development followed by diversification and novel stimulus acquisition] and brain nuclear level [multiplication of transcription factors to regulate various neuron and neuron aggregate fate to transform the spinal cord into the unique hindbrain organization]. Tying cell fate changes driven by bHLH and other transcription factors into cell and organ changes is at the moment tentative as not all relevant factors are known and their gene regulatory network is only rudimentary understood. Future research can use the blueprint proposed here to provide both the deeper molecular evolutionary understanding as well as a more detailed appreciation of developmental networks. This understanding can reveal how an auditory system evolved through transformation of existing cell fate determining networks and thus how neurosensory evolution occurred through molecular changes affecting cell fate decision processes. Appreciating the evolutionary cascade of developmental program changes could allow identifying essential steps needed to restore cells and organs in the future.

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“…Thus, beyond providing a mechanism for kinetic arrest, as seen in inert matter 52,53 , cell jamming gives rise to non-trivial biological patterns and propagation phenomena in active matter. Importantly, repulsive cell interfaces during development are often paralleled by waves and oscillations that give rise to tissue patterning 2,54,55 . Current understanding emphasizes that these waves and oscillations act upstream of boundary formation and are controlled by genetic clocks 56 .…”

mentioning

confidence: 99%

Long-lived force patterns and deformation waves at repulsive epithelial boundaries

et al. 2017

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For an organism to develop and maintain homeostasis, cell types with distinct functions must often be separated by physical boundaries. The formation and maintenance of such boundaries are commonly attributed to local mechanisms restricted to the cells lining the boundary. Here we show that, besides these local subcellular mechanisms, the formation and maintenance of tissue boundaries involves long-lived, long-ranged mechanical events. We analyzed the formation of repulsive epithelial boundaries between two epithelial monolayers, one expressing the receptor tyrosine kinase EphB2 and one expressing its ligand ephrinB1. Upon contact, both monolayers exhibited oscillatory patterns of traction forces and intercellular stresses that spanned several cell rows and tended to pull cell-matrix adhesions away from the boundary. With time, monolayers jammed and supracellular force patterns became long-lived, thereby permanently sustaining tissue segregation. Jamming was paralleled by the emergence of deformation waves that propagated away from the boundary. This phenomenon was not specific to EphB2/ephrinB1 repulsion but was also present during the formation of boundaries with an inert interface and during fusion of homotypic epithelial layers. Our findings thus unveil a global physical mechanism that sustains tissue separation independently of the biochemical and mechanical features of the local tissue boundary.

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Models for patterning primary embryonic body axes: The role of space and time

Cited by 15 publications

References 108 publications

Visualizing retinoic acid morphogen gradients

Visualizing retinoic acid morphogen gradients

Gene, cell, and organ multiplication drives inner ear evolution

Long-lived force patterns and deformation waves at repulsive epithelial boundaries

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