Cell ingression: Relevance to limb development and for adaptive evolution

Pasiliao, Clarissa C.; Hopyan, Sevan

doi:10.1002/dvg.23086

Cited by 4 publications

(4 citation statements)

References 83 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In fact, migrating MSCs represent a source of multipotent cells that are available for the repair of damaged tissues and organs (for example, bone fractures) [157]. During early vertebrate development, the migration and ingression of mesoderm-and neural crest-derived MSC initiate limb bud development [158]. Although the molecular mechanisms are still poorly understood, the limb bud identity transcription factor TBX5, which has been shown to be co-activated by YAP/TAZ in a feed-forward loop with FGFR signaling [159,160], seems to play a pivotal role [161,162].…”

Section: Yap and Taz As Regulators Of Osteogenesismentioning

confidence: 99%

The YAP/TAZ Pathway in Osteogenesis and Bone Sarcoma Pathogenesis

Kovar

Bierbaumer

Radic-Sarikas

2020

Cells

View full text Add to dashboard Cite

YAP and TAZ are intracellular messengers communicating multiple interacting extracellular biophysical and biochemical cues to the transcription apparatus in the nucleus and back to the cell/tissue microenvironment interface through the regulation of cytoskeletal and extracellular matrix components. Their activity is negatively and positively controlled by multiple phosphorylation events. Phenotypically, they serve an important role in cellular plasticity and lineage determination during development. As they regulate self-renewal, proliferation, migration, invasion and differentiation of stem cells, perturbed expression of YAP/TAZ signaling components play important roles in tumorigenesis and metastasis. Despite their high structural similarity, YAP and TAZ are functionally not identical and may play distinct cell type and differentiation stage-specific roles mediated by a diversity of downstream effectors and upstream regulatory molecules. However, YAP and TAZ are frequently looked at as functionally redundant and are not sufficiently discriminated in the scientific literature. As the extracellular matrix composition and mechanosignaling are of particular relevance in bone formation during embryogenesis, post-natal bone elongation and bone regeneration, YAP/TAZ are believed to have critical functions in these processes. Depending on the differentiation stage of mesenchymal stem cells during endochondral bone development, YAP and TAZ serve distinct roles, which are also reflected in bone tumors arising from the mesenchymal lineage at different developmental stages. Efforts to clinically translate the wealth of available knowledge of the pathway for cancer diagnostic and therapeutic purposes focus mainly on YAP and TAZ expression and their role as transcriptional co-activators of TEAD transcription factors but rarely consider the expression and activity of pathway modulatory components and other transcriptional partners of YAP and TAZ. As there is a growing body of evidence for YAP and TAZ as potential therapeutic targets in several cancers, we here interrogate the applicability of this concept to bone tumors. To this end, this review aims to summarize our current knowledge of YAP and TAZ in cell plasticity, normal bone development and bone cancer.Cells 2020, 9, 972 2 of 34 co-activators Yes-associated protein 1 (YAP-1, YAP) and its paralogue, the transcriptional co-activator with PDZ-binding motif (TAZ, WWTR1), which are typically controlled on the post-translational level by upstream regulatory signaling pathways in organ development and tissue homeostasis [2,3]. YAP and TAZ were reported to affect self-renewal and lineage commitment of stem cells [4][5][6][7], while hyperactivation of YAP and TAZ have been linked to cancer growth and metastasis in various tumors [8][9][10]. TAZ levels are elevated in approximately 20% of cancers and drive invasion and metastasis [11,12], while YAP is frequently overexpressed or amplified in cancer and was shown to promote resistance to chemotherapy in oncogene-addicted tumors up...

show abstract

Section: Yap and Taz As Regulators Of Osteogenesismentioning

confidence: 99%

The YAP/TAZ Pathway in Osteogenesis and Bone Sarcoma Pathogenesis

Kovar

Bierbaumer

Radic-Sarikas

2020

Cells

View full text Add to dashboard Cite

show abstract

“…This morphology is unlike infolding, and apically-directed migration is distinct from epithelial-mesenchymal transition ( Keller and Shook, 2011 ; Pearl et al, 2017 ). Of the two mechanisms for delamination, extrusion and ingression, early centripetal migration appears more like ingression ( Niewiadomska et al, 1999 ; Oda et al, 1997 ; Pasiliao and Hopyan, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Two phases for centripetal migration of Drosophila melanogaster follicle cells: initial ingression followed by epithelial migration

2023

View full text Add to dashboard Cite

During Drosophila oogenesis, somatic follicle cells differentiate to secrete components of the eggshell. Prior to secretion, the epithelium reorganizes to shape eggshell specializations, including border FC collective cell migration and later dorsal formation. These FC movements provide valuable insights into collective cell migration. However, little is known about centripetal migration, which encloses the oocyte after secretion has begun. Centripetal migration begins with apical extension of a few follicle cells (FCs) that move away from the basement membrane to invade between germ cells. We define a timeline of reproducible milestones, using time-lapse imaging of egg chamber explants. Inward migration occurs in two phases. First, leading centripetal FCs ingress, extending apically over the anterior oocyte, and constricting basally. Second, following FCs move collectively toward the anterior, then around the corner to move inward with minimal change in aspect ratio. E-Cadherin was required in leading centripetal FCs for their normal ingression, assessed with homozygous shotgun mutant or RNAi knockdown clones; ingression was influenced non-autonomously by mutant following FCs. This work establishes centripetal migration as an accessible model for biphasic, E-Cadherin-adhesion mediated, collective migration.

show abstract

“…Cell ingression among vertebrates may have been adapted from ancient invertebrate cell behaviours observed at the archenteron margin in diploblasts 7,91,92 . As has been suggested, a small number of conserved physical rules may underlie basic morphogenetic motifs that were diversified by genetic variations 16,93 .…”

Section: Discussionmentioning

confidence: 99%

Fluctuations and entropy enable neural crest cell ingression

Pasiliao

Thomas

Yung

et al. 2023

Preprint

Self Cite

View full text Add to dashboard Cite

The second law of thermodynamics explains the dissipative nature of embryonic development as an exchange of energy-dependent order for proportionately greater output of heat and waste. Recent work on granular matter provides a path by which to define the roles of passive, stochastic mechanisms in nonequilibrium systems. Here, we apply such a framework to examine the role of thermodynamic parameters to cell ingression, the movement of cells from one tissue layer to another that has been attributed, in part, to directional cues. Using the murine neural crest as a model system, we provide evidence that a stochastic mechanism, rather than a proposed stiffness gradient, underlies cell ingression. Cortical fluctuations representing effective temperature and cell packing configurations generate an entropic trap that promotes cell ingression. The results imply dissipative mechanisms that transiently disorder tissue underlie some morphogenetic events.

show abstract

Cell ingression: Relevance to limb development and for adaptive evolution

Cited by 4 publications

References 83 publications

The YAP/TAZ Pathway in Osteogenesis and Bone Sarcoma Pathogenesis

The YAP/TAZ Pathway in Osteogenesis and Bone Sarcoma Pathogenesis

Two phases for centripetal migration of Drosophila melanogaster follicle cells: initial ingression followed by epithelial migration

Fluctuations and entropy enable neural crest cell ingression

Contact Info

Product

Resources

About