Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Molecular consequences of Dlx3 deletion in mouse enamel organ as determined by RNASeq analysis

ABSTRACT: DLX3 is a homeodomain transcription factor involved in ameloblast differentiation and enamel formation. Mutations in DLX3 in human lead to defects in enamel. However, the downstream targets of Dlx3 transcriptional activity in the enamel organ have not been identified yet. In this study, we compared the transcriptome of enamel organs where Dlx3 has been deleted to control tissues. Total RNA was extracted from enamel organs (mandibular incisors) from Dlx3-WT (N=4) and Dlx3-K14cKO (N=4) mice at P10. cDNA libraries were generated using NEBnext and NuGen kits. Sequencing was performed on the HiSeq2000.

ORGANISM(S): Mus musculus

SUBMITTER: Hong-wei Sun

PROVIDER: E-GEOD-57984 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Hair keratin mutations in tooth enamel increase dental decay risk.

Duverger Olivier O Ohara Takahiro T Shaffer John R JR Donahue Danielle D Zerfas Patricia P Dullnig Andrew A Crecelius Christopher C Beniash Elia E Marazita Mary L ML Morasso Maria I MI

The Journal of clinical investigation 20141027 12

Tooth enamel is the hardest substance in the human body and has a unique combination of hardness and fracture toughness that protects teeth from dental caries, the most common chronic disease worldwide. In addition to a high mineral content, tooth enamel comprises organic material that is important for mechanical performance and influences the initiation and progression of caries; however, the protein composition of tooth enamel has not been fully characterized. Here, we determined that epitheli ...[more]

PMID: 25347471

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Project description:In a systemic effort to survive environmental stress, organ systems fluctuate and adapt to overcome external pressures. The evolutionary drive back towards homeostasis, makes it difficult to determine if an organism experienced a toxic exposure to stress, especially in early prenatal and neonatal periods of development. Previous studies indicate that primary human teeth may provide historical records of experiences related to stressors during that early time window. To assess the molecular effects of early life adversity on enamel formation, we used a limited bedding and nesting (LBN) mouse model of early life adversity (ELA), to assess changes in enamel organ gene expression and enamel mineralization. Enamel of postnatal day 12 (P12) weight-matched ELA mice was more mineralized as compared control enamel. RNAseq showed 724 genes significantly upregulated in ELA enamel organs as compared to controls, and 574 significantly downregulated genes (DESeq2 p-value <= 0.05). Transcripts expressing the enamel matrix proteins amelogenin (Amelx) and enamelin (Enam) were among the top 4 most differentially expressed genes. The most significantly enriched GO and Reactome pathway was Extracellular Matrix Organization, while the most significantly enriched KEGG Pathways were Butanoate metabolism and Synthesis and Degradation of Ketone Bodies. qPCR analysis of weight-matched ELA and control enamel organs confirmed that expression of the ameloblast-specific proteins Amelx and Enam were highly upregulated in ELA mice. When evaluating molecular mechanisms for amelogenin upregulation, we found significantly increased expression of Dlx3, while transcripts for clock genes Per1 and Nrd1, which have also positively associated with amelogenin expression, were downregulated. These findings suggest that the developing enamel organs are sensitive to the pressures of early life adversity and produce structural biomarkers in tooth enamel mineral to reflect these changes. Together these results support the possibility that tooth enamel may contain biomarkers of cellular effects associated with systemic early life adversity.

Dataset Information

Molecular consequences of Dlx3 deletion in mouse enamel organ as determined by RNASeq analysis

Publications

Hair keratin mutations in tooth enamel increase dental decay risk.

Similar Datasets

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