Identification of oscillatory genes in somitogenesis from functional genomic analysis of a human mesenchymal stem cell model

William, Dilusha A.; Saitta, B.; Gibson, Joshua D.; Traas, Jeremy; Markov, Vladimir; Gonzalez, Dorian M.; Sewell, William F.; Anderson, D.M.W.; Pratt, Stephen C.; Rappaport, Eric; Kusumi, Kenro

doi:10.1016/j.ydbio.2007.02.007

Cited by 63 publications

(46 citation statements)

References 66 publications

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“…The segmentation clock period varies widely between species, consistent with their differing developmental paces. For example, the segmentation clock oscillates about threefold more slowly in humans than in mice (39,40). To study species-specific differences in more detail, we analyzed splicing and export delays in chicken embryos, whose segmentation clock is about 30 min shorter than in mice.…”

Section: Resultsmentioning

confidence: 99%

Transcript processing and export kinetics are rate-limiting steps in expressing vertebrate segmentation clock genes

Hoyle

Ish‐Horowicz

2013

Proc. Natl. Acad. Sci. U.S.A.

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Sequential production of body segments in vertebrate embryos is regulated by a molecular oscillator (the segmentation clock) that drives cyclic transcription of genes involved in positioning intersegmental boundaries. Mathematical modeling indicates that the period of the clock depends on the total delay kinetics of a negative feedback circuit, including those associated with the synthesis of transcripts encoding clock components [Lewis J (2003) Curr Biol 13(16):1398-1408]. Here, we measure expression delays for three transcripts [Lunatic fringe, Hes7/her1, and Notch-regulatedankyrin-repeat-protein (Nrarp)], that cycle during segmentation in the zebrafish, chick, and mouse, and provide in vivo measurements of endogenous splicing and export kinetics. We show that mRNA splicing and export are much slower than transcript elongation, with the longest delay (about 16 min in the mouse) being due to mRNA export. We conclude that the kinetics of mRNA and protein production and destruction can account for much of the clock period, and provide strong support for delayed autorepression as the underlying mechanism of the segmentation clock.transcriptional delays | RNA export | RNA splicing | mRNA processing | somites

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Section: Resultsmentioning

confidence: 99%

Transcript processing and export kinetics are rate-limiting steps in expressing vertebrate segmentation clock genes

Hoyle

Ish‐Horowicz

2013

Proc. Natl. Acad. Sci. U.S.A.

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“…HES1 transcription is oscillated in many cell types, such as fibroblasts, myoblasts, neuroblasts, and mesenchymal stem cells (51,52). Human HES1 is oscillated with a period of 5 h, while mouse Hes1 is oscillated with a period of 2 h (52).…”

Section: Discussionmentioning

confidence: 99%

Integrative genomic analyses on HES/HEY family: Notch-independent HES1, HES3 transcription in undifferentiated ES cells, and Notch-dependent HES1, HES5, HEY1, HEY2, HEYL transcription in fetal tissues, adult tissues, or cancer

Katoh¹,

Katoh²

2007

Int J Oncol

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Abstract. Notch signaling pathway maintains stem cells through transcriptional activation of HES/HEY family members to repress tissue-specific transcription factors. Here, comparative integromic analyses on HES/HEY family members were carried out. HES3 gene encodes two isoforms due to alternative promoters. Complete coding sequence of HES3 variant 2 was determined by curating CX755241.1 EST. Refined phylogenetic analysis using HES3 variant 2 instead of variant 1 revealed that mammalian bHLH transcription factors with Orange domain were grouped into HES subfamily (HES1, HES2, HES3, HES4, HES5, HES6, HES7) and HEY subfamily (HEY1, HEY2, HEYL, HESL/HELT, DEC1/ BHLHB2, DEC2/BHLHB3). Eight amino-acid residues were added to the C-terminal WRPW motif in human HES3 due to lineage specific T to G nucleotide change at stop codon of chimpanzee, rat, and mouse HES3 orthologs. HES1 and HES3 were expressed in undifferentiated embryonic stem (ES) cells. HES1 was also expressed in fetal tissues, and regenerating liver. HES1, HEY1 and HEY2 were expressed in endothelial cells. HES1, HES4 and HES6 were expressed in gastric cancer, HES1 and DEC1 in pancreatic cancer, HES1, HES2, HES4, HES6 and DEC2 in colorectal cancer. HES6 was also expressed in other tumors, such as brain tumors, melanoma, small cell lung cancer, retinoblastoma, ovarian cancer, and breast cancer. Double NANOG-binding sites, CSL/ RBPSUH-binding site and TATA-box in HES1 promoter, NANOG-, SOX2-, POU5F1/OCT3/OCT4-binding sites and TATA-box in HES3 promoter, double CSL-binding sites in HES5 promoter, SOX2-, POU-binding sites and TATA-box in HES6 promoter, and CSL-binding site in HEY1, HEY2 and HEYL promoters were evolutionarily conserved. However, double CSL-binding sites in mouse Hes7 promoter were not conserved in human HES7 promoter. Together these facts indicate that HES1 and HES3 were target genes of the ES cellspecific network of transcription factors, and that HES1, HES5, HEY1, HEY2 and HEYL were target genes of Notch signaling pathway.

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“…Recently, ECM has been recognized for its critical roles to maintain a special local environment for adult stem cells, stem cell niche, and ECM degradation involved in stem cell differentiation, activation, and/or release (William, 2007;Chen, 2010;Reilly and Engler, 2010). Degradation of the ECM by proteases would break contacts between ECM molecules and integrin receptors, leading to changes in cell shape and reorganization of the actin cytoskeleton (Juliano and Haskill, 1993).…”

Section: Ecm Degradation and Dedifferentiationmentioning

confidence: 99%

Matrix metalloproteinase expression during blastema formation in regeneration‐competent versus regeneration‐deficient amphibian limbs

Santosh

Windsor

Mahmoudi

et al. 2010

Developmental Dynamics

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We used an antibody array to compare the protein expression of matrix metalloproteinases (MMPs)-1, -2, -3, -8, -9, -10, and -13, as well as the tissue inhibitors of metalloproteinases (TIMPs)-1, -2, and -4 during blastema formation in amputated hindlimbs of regeneration-competent wild-type axolotls and stage-54 Xenopus, and regeneration-deficient short-toes axolotls and Xenopus froglets. Expression of MMP-9 and -2 was also compared by zymography. Both short-toes and froglet failed to up-regulate MMPs in a pattern comparable to the wild-type axolotl, suggesting that subnormal histolysis is at least in part responsible for the poor blastema formation characteristic of both short-toes and froglet. MMP levels were much lower in amputated stage-54 Xenopus limb buds than in the other animals, suggesting that blastema formation in these limb buds requires much less extracellular matrix degradation than in fully differentiated limbs. TIMP expression patterns followed the same trends as the MMP's in each group of animals. Developmental

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Identification of oscillatory genes in somitogenesis from functional genomic analysis of a human mesenchymal stem cell model

Cited by 63 publications

References 66 publications

Transcript processing and export kinetics are rate-limiting steps in expressing vertebrate segmentation clock genes

Transcript processing and export kinetics are rate-limiting steps in expressing vertebrate segmentation clock genes

Integrative genomic analyses on HES/HEY family: Notch-independent HES1, HES3 transcription in undifferentiated ES cells, and Notch-dependent HES1, HES5, HEY1, HEY2, HEYL transcription in fetal tissues, adult tissues, or cancer

Matrix metalloproteinase expression during blastema formation in regeneration‐competent versus regeneration‐deficient amphibian limbs

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