Search engine for discovering works of Art, research articles, and books related to Art and Culture
ShareThis
Javascript must be enabled to continue!

C‐Jun N‐terminal Kinase (JNK) maintains tissue integrity during cell rearrangement in the gut

View through CrossRef
Tissue elongation is a fundamental morphogenetic process that generates the proper anatomical topology of the body plan and vital organs. In vertebrates, c‐Jun N‐terminal Kinase (JNK) is a downstream effector of Wnt/PCP signaling that is required for tissue elongation, but the precise cellular role of JNK in this context has remained elusive. Here, we show that JNK activity is indispensable for the rearrangement of endoderm cells that underlies the elongation of the Xenopus gut tube. Whereas other Wnt/PCP mediators, such as Rho, are necessary to induce cell intercalation and remodel adhesive contacts, we found that JNK is required to maintain cell‐cell adhesion and establish parallel microtubule arrays; without JNK activity, the reorganizing endoderm dissociates. Depleting microtubules phenocopies JNK inhibition, consistent with a model in which JNK regulates microtubule architecture to preserve adhesive contacts between rearranging cells. Thus, in contrast to Rho, which generates actomyosin‐based tension and cell movement, JNK signaling is required to establish cytoskeletal stability and maintain tissue cohesion; both factors are required to achieve proper cell rearrangement and gut extension. Our results shed new light on the means by which intra‐ and intercellular forces are balanced to promote topological change, while preserving structural integrity, in numerous morphogenetic contexts.
Title: C‐Jun N‐terminal Kinase (JNK) maintains tissue integrity during cell rearrangement in the gut
Description:
Tissue elongation is a fundamental morphogenetic process that generates the proper anatomical topology of the body plan and vital organs.
In vertebrates, c‐Jun N‐terminal Kinase (JNK) is a downstream effector of Wnt/PCP signaling that is required for tissue elongation, but the precise cellular role of JNK in this context has remained elusive.
Here, we show that JNK activity is indispensable for the rearrangement of endoderm cells that underlies the elongation of the Xenopus gut tube.
Whereas other Wnt/PCP mediators, such as Rho, are necessary to induce cell intercalation and remodel adhesive contacts, we found that JNK is required to maintain cell‐cell adhesion and establish parallel microtubule arrays; without JNK activity, the reorganizing endoderm dissociates.
Depleting microtubules phenocopies JNK inhibition, consistent with a model in which JNK regulates microtubule architecture to preserve adhesive contacts between rearranging cells.
Thus, in contrast to Rho, which generates actomyosin‐based tension and cell movement, JNK signaling is required to establish cytoskeletal stability and maintain tissue cohesion; both factors are required to achieve proper cell rearrangement and gut extension.
Our results shed new light on the means by which intra‐ and intercellular forces are balanced to promote topological change, while preserving structural integrity, in numerous morphogenetic contexts.

Related Results

JNK Pathway Is Constitutively Activated and Is Required for Survival in Human Mantle-Cell Lymphoma Fresh Cells and Cell-Lines.
JNK Pathway Is Constitutively Activated and Is Required for Survival in Human Mantle-Cell Lymphoma Fresh Cells and Cell-Lines.
Abstract We previously reported that GST-pi, a cellular JNK effector and activator, was strongly expressed in MCL patient’s samples (Clin Cancer Res. 2004). Recently...
Optogenetic Control of Spine-Head JNK Reveals a Role in Dendritic Spine Regression
Optogenetic Control of Spine-Head JNK Reveals a Role in Dendritic Spine Regression
AbstractIn this study, we use an optogenetic inhibitor of c-Jun NH2-terminal kinase (JNK) in dendritic spine sub-compartments of rat hippocampal neurons. We show that JNK inhibitio...
ROLE OF HMGB1 IN DOXORUBICIN-INDUCED MYOCARDIAL APOPTOSIS AND ITS REGULATION PATHWAY
ROLE OF HMGB1 IN DOXORUBICIN-INDUCED MYOCARDIAL APOPTOSIS AND ITS REGULATION PATHWAY
Objectives Doxorubicin (DOX) is a widely used anti-tumour agent. The clinical application of the medication is limited by its side effect which can elicit myocard...
SUMMARY
SUMMARY
SUMMARYThe purpose of the present monograph is to give an account of the distribution of fibrinolytic components in the organism, with special reference to the tissue activator of ...
Developing guidelines for research institutions
Developing guidelines for research institutions
As introduced in Chapter 1, in this thesis, I developed guidelines to research institutions on how to foster research integrity. I did this by exploring how research institutions c...
c-Jun N-terminal kinase – c-Jun pathway transactivates Bim to promote osteoarthritis
c-Jun N-terminal kinase – c-Jun pathway transactivates Bim to promote osteoarthritis
Osteoarthritis (OA) is a chronic degenerative joint disorder. Previous studies have shown abnormally increased apoptosis of chondrocytes in patients and animal models of OA. TNF-α ...
Characterization of a microtubule‐associated protein, doublecortin (DCX), as a substrate of c‐Jun N‐terminal Kinases (JNKs)
Characterization of a microtubule‐associated protein, doublecortin (DCX), as a substrate of c‐Jun N‐terminal Kinases (JNKs)
We are interested how docking motifs contribute to substrate recognition by JNK, a Ser/Thr protein kinase and member of the Mitogen‐Activated Protein Kinase (MAPK) family. The acti...

Back to Top