scholarly journals A gene regulatory network for apical organ neurogenesis and its spatial control in sea star embryos.

2016 ◽  
Author(s):  
Alys Jarvela ◽  
Kristen Yankura ◽  
Veronica Hinman
Keyword(s):  
Regulatory Network ◽  
Apical Organ ◽  
Spatial Patterning ◽  
Sea Star ◽  
Spatial Control ◽  
Neural Fate ◽  
Multipotent Progenitors ◽  
Asymmetric Divisions ◽  
Gene Regulatory ◽  
Anterior Posterior

How neural stem cells generate the correct number and type of differentiated neurons in appropriate places is an important question in developmental biology. Although nervous systems are diverse across phyla, many taxa have a larva that forms an anterior concentration of neurons, or apical organ. The number of neurons in these organs is highly variable. We show that neurogenesis in the sea star larvae begins with soxc-expressing multipotent progenitors. These give rise to restricted progenitors that express lhx2/9. Soxc- and lhx2/9-expressing cells are capable of undergoing both asymmetric divisions, which allow for progression towards a particular neural fate, and symmetric proliferative divisions. Nested concentric domains of gene expression along the anterior-posterior (AP) axis, which have been observed in a great diversity of metazoans, control neurogenesis in the sea star by promoting particular division modes and progression towards becoming a neuron. This work, therefore, explains how spatial patterning in the ectoderm controls progression of neurogenesis. Modification to the sizes of these AP territories provides a simple mechanism to explain the diversity of neuron number found among apical organs.

scholarly journals A gene regulatory network for apical organ neurogenesis and its spatial control in sea star embryos

Development ◽  
2016 ◽  
Vol 143 (22) ◽  
pp. 4214-4223 ◽  
Author(s):  
Alys M. Cheatle Jarvela ◽  
Kristen A. Yankura ◽  
Veronica F. Hinman
Keyword(s):  
Gene Regulatory Network ◽  
Regulatory Network ◽  
Apical Organ ◽  
Sea Star ◽  
Spatial Control ◽  
Gene Regulatory

scholarly journals Embryonic geometry underlies phenotypic variation in decanalized conditions

2019 ◽  
Author(s):  
A. Huang ◽  
T. E. Saunders
Keyword(s):  
Phenotypic Variation ◽  
Regulatory Network ◽  
Physical Space ◽  
Model Organisms ◽  
Wild Type ◽  
Environmental Perturbations ◽  
Key Factor ◽  
In The Wild ◽  
Gene Regulatory ◽  
Anterior Posterior

AbstractDuring development, many mutations cause increased variation in phenotypic outcomes, a phenomenon termed decanalization. Such variations can often be attributed to genetic and environmental perturbations. However, phenotypic discordance remains even in isogenic model organisms raised in homogeneous environments. To understand the mechanisms underlying phenotypic variation, we used as a model the highly precise anterior-posterior (AP) patterning of the early Drosophila embryo. We decanalized the system by depleting the maternal bcd product and found that in contrast to the highly scaled patterning in the wild-type, the segmentation gene boundaries shift away from the scaled positions according to the total embryonic length. Embryonic geometry is hence a key factor predetermining patterning outcomes in such decanalized conditions. Embryonic geometry was also found to predict individual patterning outcomes under bcd overexpression, another decanalizing condition. Further analysis of the gene regulatory network acting downstream of the morphogen identified vulnerable points in the networks due to limitations in the available physical space.

scholarly journals The MITF paralog tfec is required in neural crest development for fate specification of the iridophore lineage from a multipotent pigment cell progenitor

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0244794 ◽  
Author(s):  
Kleio Petratou ◽  
Samantha A. Spencer ◽  
Robert N. Kelsh ◽  
James A. Lister
Keyword(s):  
Neural Crest ◽  
Regulatory Network ◽  
Pigment Cell ◽  
Cell Types ◽  
Cellular Mechanisms ◽  
Cell Fates ◽  
Master Regulator ◽  
Fate Specification ◽  
Multipotent Progenitors ◽  
Gene Regulatory

Understanding how fate specification of distinct cell-types from multipotent progenitors occurs is a fundamental question in embryology. Neural crest stem cells (NCSCs) generate extraordinarily diverse derivatives, including multiple neural, skeletogenic and pigment cell fates. Key transcription factors and extracellular signals specifying NCSC lineages remain to be identified, and we have only a little idea of how and when they function together to control fate. Zebrafish have three neural crest-derived pigment cell types, black melanocytes, light-reflecting iridophores and yellow xanthophores, which offer a powerful model for studying the molecular and cellular mechanisms of fate segregation. Mitfa has been identified as the master regulator of melanocyte fate. Here, we show that an Mitf-related transcription factor, Tfec, functions as master regulator of the iridophore fate. Surprisingly, our phenotypic analysis of tfec mutants demonstrates that Tfec also functions in the initial specification of all three pigment cell-types, although the melanocyte and xanthophore lineages recover later. We show that Mitfa represses tfec expression, revealing a likely mechanism contributing to the decision between melanocyte and iridophore fate. Our data are consistent with the long-standing proposal of a tripotent progenitor restricted to pigment cell fates. Moreover, we investigate activation, maintenance and function of tfec in multipotent NCSCs, demonstrating for the first time its role in the gene regulatory network forming and maintaining early neural crest cells. In summary, we build on our previous work to characterise the gene regulatory network governing iridophore development, establishing Tfec as the master regulator driving iridophore specification from multipotent progenitors, while shedding light on possible cellular mechanisms of progressive fate restriction.

scholarly journals The MITF paralog tfec is required in neural crest development for fate specification of the iridophore lineage from a multipotent pigment cell progenitor

2019 ◽  
Author(s):  
K. Petratou ◽  
S. A. Spencer ◽  
R. N. Kelsh ◽  
J. A. Lister
Keyword(s):  
Neural Crest ◽  
Regulatory Network ◽  
Pigment Cell ◽  
Cell Types ◽  
Cellular Mechanisms ◽  
Cell Fates ◽  
Master Regulator ◽  
Fate Specification ◽  
Multipotent Progenitors ◽  
Gene Regulatory

Understanding how fate specification of distinct cell-types from multipotent progenitors occurs is a fundamental question in embryology. Neural crest stem cells (NCSCs) generate extraordinarily diverse derivatives, including multiple neural, skeletogenic and pigment cell fates. Key transcription factors and extracellular signals specifying NCSC lineages remain to be identified, and we have only a little idea of how and when they function together to control fate. Zebrafish have three neural crest-derived pigment cell types, black melanocytes, light-reflecting iridophores and yellow xanthophores, which offer a powerful model for studying the molecular and cellular mechanisms of fate segregation. Mitfa has been identified as the master regulator of melanocyte fate. Here, we show that an Mitf-related transcription factor, Tfec, functions as master regulator of the iridophore fate. Surprisingly, our phenotypic analysis of tfec mutants demonstrates that Tfec also functions in the initial specification of all three pigment cell-types, although the melanocyte and xanthophore lineages recover later. We show that Mitfa represses tfec expression, revealing a likely mechanism contributing to the decision between melanocyte and iridophore fate. Our data is consistent with the long-standing proposal of a tripotent progenitor restricted to pigment cell fates. Moreover, we investigate activation, maintenance and function of tfec in multipotent NCSCs, demonstrating for the first time its role in the gene regulatory network forming and maintaining early neural crest cells. In summary, we build on our previous work to characterise the gene regulatory network governing iridophore development, establishing Tfec as the master regulator driving iridophore specification from multipotent progenitors, while shedding light on possible cellular mechanisms of progressive fate restriction.

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