Bar-1 loss-of-function causes a developmental delay in intertwined with a DAF-16 stress response

M.G. Sterken, M.L. van der Bent, R.J.M. Volkers, J.A.G. Riksen, T. Schmid, A. Hajnal, J.E. Kammenga, L.B. Snoek

Research output: Chapter in Book/Report/Conference proceedingAbstract

Abstract

The Wnt/â-catenin pathway is a key development pathway in metazoans. C. elegans has been extensively used as a model species to study the Wnt pathway. Four â-catenins in C. elegans are important gene expression regulators in Wnt signalling. One of these, bar-1, is part of the canonical Wnt pathway. Together with Wnt effector POP-1, BAR-1 forms a transcription activation complex which regulates the transcription of downstream genes. The effects of bar-1 loss-of-function mutations on many phenotypes, like vulval development and neuronal migration, have been studied well. However, the effects on global gene expression remain largely unknown. The transcriptional profiles of the strain EW15, carrying bar-1(ga80)lof, and Bristol N2 were measured in the L4 stage of age-synchronized populations at 48 hours. Gene expression differences were combines whit ChiP-seq data from the modENCODE project to pinpoint involved transcription factors. Genes differentially expressed between EW15 and N2 showed strong signs that development of bar-1(ga80)lof was slowed down. We verified this observation by measuring the timing of egg-hatching and egg-laying. The development delay increased over time, ranging from 0 hours at the moment of egg-hatching to 6 hours at the moment of the egg laying. After correcting for this development delay, gene expression analysis revealed that the expression of many genes involved in the Wnt pathway were activated in the bar-1 mutant. Furthermore, the genes up-regulated in the bar-1 mutant showed enrichment for transcription factor activity. These up-regulated genes show strong indications of DAG-16 involvement by the combination of modENCODE ChiP-seq data as well as known DAF-16 regulated genes. Together our findings show that bar-1 loss-of-function leads to delayed development and an activated Wnt pathway, and indicate that the DAF-16 stress-response is causative of this development delay.
Original languageEnglish
Title of host publicationProceedings of the Berlin C. elegans Meeting 2014
Pages241-241
Publication statusPublished - 2014
EventBerlin C. elegans Meeting 2014, Berlin, Germany -
Duration: 15 May 201417 May 2014

Conference

ConferenceBerlin C. elegans Meeting 2014, Berlin, Germany
Period15/05/1417/05/14

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Wnt Signaling Pathway
Ovum
Gene Expression
Catenins
Genes
Transcription Factors
Transcriptional Activation
Phenotype
Mutation
Population

Cite this

Sterken, M. G., van der Bent, M. L., Volkers, R. J. M., Riksen, J. A. G., Schmid, T., Hajnal, A., ... Snoek, L. B. (2014). Bar-1 loss-of-function causes a developmental delay in intertwined with a DAF-16 stress response. In Proceedings of the Berlin C. elegans Meeting 2014 (pp. 241-241)
Sterken, M.G. ; van der Bent, M.L. ; Volkers, R.J.M. ; Riksen, J.A.G. ; Schmid, T. ; Hajnal, A. ; Kammenga, J.E. ; Snoek, L.B. / Bar-1 loss-of-function causes a developmental delay in intertwined with a DAF-16 stress response. Proceedings of the Berlin C. elegans Meeting 2014. 2014. pp. 241-241
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title = "Bar-1 loss-of-function causes a developmental delay in intertwined with a DAF-16 stress response",
abstract = "The Wnt/{\^a}-catenin pathway is a key development pathway in metazoans. C. elegans has been extensively used as a model species to study the Wnt pathway. Four {\^a}-catenins in C. elegans are important gene expression regulators in Wnt signalling. One of these, bar-1, is part of the canonical Wnt pathway. Together with Wnt effector POP-1, BAR-1 forms a transcription activation complex which regulates the transcription of downstream genes. The effects of bar-1 loss-of-function mutations on many phenotypes, like vulval development and neuronal migration, have been studied well. However, the effects on global gene expression remain largely unknown. The transcriptional profiles of the strain EW15, carrying bar-1(ga80)lof, and Bristol N2 were measured in the L4 stage of age-synchronized populations at 48 hours. Gene expression differences were combines whit ChiP-seq data from the modENCODE project to pinpoint involved transcription factors. Genes differentially expressed between EW15 and N2 showed strong signs that development of bar-1(ga80)lof was slowed down. We verified this observation by measuring the timing of egg-hatching and egg-laying. The development delay increased over time, ranging from 0 hours at the moment of egg-hatching to 6 hours at the moment of the egg laying. After correcting for this development delay, gene expression analysis revealed that the expression of many genes involved in the Wnt pathway were activated in the bar-1 mutant. Furthermore, the genes up-regulated in the bar-1 mutant showed enrichment for transcription factor activity. These up-regulated genes show strong indications of DAG-16 involvement by the combination of modENCODE ChiP-seq data as well as known DAF-16 regulated genes. Together our findings show that bar-1 loss-of-function leads to delayed development and an activated Wnt pathway, and indicate that the DAF-16 stress-response is causative of this development delay.",
author = "M.G. Sterken and {van der Bent}, M.L. and R.J.M. Volkers and J.A.G. Riksen and T. Schmid and A. Hajnal and J.E. Kammenga and L.B. Snoek",
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Sterken, MG, van der Bent, ML, Volkers, RJM, Riksen, JAG, Schmid, T, Hajnal, A, Kammenga, JE & Snoek, LB 2014, Bar-1 loss-of-function causes a developmental delay in intertwined with a DAF-16 stress response. in Proceedings of the Berlin C. elegans Meeting 2014. pp. 241-241, Berlin C. elegans Meeting 2014, Berlin, Germany, 15/05/14.

Bar-1 loss-of-function causes a developmental delay in intertwined with a DAF-16 stress response. / Sterken, M.G.; van der Bent, M.L.; Volkers, R.J.M.; Riksen, J.A.G.; Schmid, T.; Hajnal, A.; Kammenga, J.E.; Snoek, L.B.

Proceedings of the Berlin C. elegans Meeting 2014. 2014. p. 241-241.

Research output: Chapter in Book/Report/Conference proceedingAbstract

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T1 - Bar-1 loss-of-function causes a developmental delay in intertwined with a DAF-16 stress response

AU - Sterken, M.G.

AU - van der Bent, M.L.

AU - Volkers, R.J.M.

AU - Riksen, J.A.G.

AU - Schmid, T.

AU - Hajnal, A.

AU - Kammenga, J.E.

AU - Snoek, L.B.

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N2 - The Wnt/â-catenin pathway is a key development pathway in metazoans. C. elegans has been extensively used as a model species to study the Wnt pathway. Four â-catenins in C. elegans are important gene expression regulators in Wnt signalling. One of these, bar-1, is part of the canonical Wnt pathway. Together with Wnt effector POP-1, BAR-1 forms a transcription activation complex which regulates the transcription of downstream genes. The effects of bar-1 loss-of-function mutations on many phenotypes, like vulval development and neuronal migration, have been studied well. However, the effects on global gene expression remain largely unknown. The transcriptional profiles of the strain EW15, carrying bar-1(ga80)lof, and Bristol N2 were measured in the L4 stage of age-synchronized populations at 48 hours. Gene expression differences were combines whit ChiP-seq data from the modENCODE project to pinpoint involved transcription factors. Genes differentially expressed between EW15 and N2 showed strong signs that development of bar-1(ga80)lof was slowed down. We verified this observation by measuring the timing of egg-hatching and egg-laying. The development delay increased over time, ranging from 0 hours at the moment of egg-hatching to 6 hours at the moment of the egg laying. After correcting for this development delay, gene expression analysis revealed that the expression of many genes involved in the Wnt pathway were activated in the bar-1 mutant. Furthermore, the genes up-regulated in the bar-1 mutant showed enrichment for transcription factor activity. These up-regulated genes show strong indications of DAG-16 involvement by the combination of modENCODE ChiP-seq data as well as known DAF-16 regulated genes. Together our findings show that bar-1 loss-of-function leads to delayed development and an activated Wnt pathway, and indicate that the DAF-16 stress-response is causative of this development delay.

AB - The Wnt/â-catenin pathway is a key development pathway in metazoans. C. elegans has been extensively used as a model species to study the Wnt pathway. Four â-catenins in C. elegans are important gene expression regulators in Wnt signalling. One of these, bar-1, is part of the canonical Wnt pathway. Together with Wnt effector POP-1, BAR-1 forms a transcription activation complex which regulates the transcription of downstream genes. The effects of bar-1 loss-of-function mutations on many phenotypes, like vulval development and neuronal migration, have been studied well. However, the effects on global gene expression remain largely unknown. The transcriptional profiles of the strain EW15, carrying bar-1(ga80)lof, and Bristol N2 were measured in the L4 stage of age-synchronized populations at 48 hours. Gene expression differences were combines whit ChiP-seq data from the modENCODE project to pinpoint involved transcription factors. Genes differentially expressed between EW15 and N2 showed strong signs that development of bar-1(ga80)lof was slowed down. We verified this observation by measuring the timing of egg-hatching and egg-laying. The development delay increased over time, ranging from 0 hours at the moment of egg-hatching to 6 hours at the moment of the egg laying. After correcting for this development delay, gene expression analysis revealed that the expression of many genes involved in the Wnt pathway were activated in the bar-1 mutant. Furthermore, the genes up-regulated in the bar-1 mutant showed enrichment for transcription factor activity. These up-regulated genes show strong indications of DAG-16 involvement by the combination of modENCODE ChiP-seq data as well as known DAF-16 regulated genes. Together our findings show that bar-1 loss-of-function leads to delayed development and an activated Wnt pathway, and indicate that the DAF-16 stress-response is causative of this development delay.

M3 - Abstract

SP - 241

EP - 241

BT - Proceedings of the Berlin C. elegans Meeting 2014

ER -

Sterken MG, van der Bent ML, Volkers RJM, Riksen JAG, Schmid T, Hajnal A et al. Bar-1 loss-of-function causes a developmental delay in intertwined with a DAF-16 stress response. In Proceedings of the Berlin C. elegans Meeting 2014. 2014. p. 241-241