ALTERED MERISTEM PROGRAM1 (AMP1) is a member of the M28 family of carboxypeptidases with a pivotal role in cell fate maintenance in the embryo and shoot meristem. A defect in AMP1 function results in suspensor to embryo conversion and a hypertrophic shoot meristem forming ectopic stem cell pools. However, so far the role of AMP1 in shoot development could not be assigned to a specific molecular pathway nor is its biochemical function resolved. Double mutants in CYP78A5 and CYP78A7 develop a similar set of cell fate defects. To further assess whether this phenotypic overlap is also depicted in a congruency at the global gene expression level, we analyzed the transcriptomic responses of both genotypes
AMP1 and CYP78A5/7 act through a common pathway to govern cell fate maintenance in Arabidopsis thaliana.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The Small Molecule Hyperphyllin Enhances Leaf Formation Rate and Mimics Shoot Meristem Integrity Defects Associated with AMP1 Deficiency.
Specimen part, Treatment
View SamplesALTERED MERISTEM PROGRAM1 (AMP1) is a member of the M28 family of carboxypeptidases with a pivotal role in plant development and stress adaptation. Its most prominent mutant defect is a unique hypertrophic shoot phenotype combining a strongly increased organ formation rate with enhanced meristem size and the formation of ectopic meristem poles. However, so far the role of AMP1 in shoot development could not be assigned to a specific molecular pathway nor is its biochemical function resolved. We used a chemical genetic approach to identify the drug hyperphyllin (HP), which specifically mimics the shoot defects of amp1, including plastochron reduction and enlargement and multiplication of the shoot meristem. To further assess whether hyperphyllin acts in an AMP1-dependent manner we compared the transcriptonal responses of hyperphyllin-treated wild-type and amp1 mutant seedlings.
The Small Molecule Hyperphyllin Enhances Leaf Formation Rate and Mimics Shoot Meristem Integrity Defects Associated with AMP1 Deficiency.
Specimen part, Treatment
View SamplesALTERED MERISTEM PROGRAM1 (AMP1) is a member of the M28 family of carboxypeptidases with a pivotal role in plant development and stress adaptation. Its most prominent mutant defect is a unique hypertrophic shoot phenotype combining a strongly increased organ formation rate with enhanced meristem size and the formation of ectopic meristem poles. However, so far the role of AMP1 in shoot development could not be assigned to a specific molecular pathway nor is its biochemical function resolved. We used a chemical genetic approach to identify the drug hyperphyllin (HP), which specifically mimics the shoot defects of amp1, including plastochron reduction and enlargement and multiplication of the shoot meristem. To further assess whether hyperphyllin acts in an AMP1-dependent manner we compared the transcriptonal responses of hyperphyllin-treated wild-type Arabidopsis seedlings with those of untreated amp1 mutant seedlings.
The Small Molecule Hyperphyllin Enhances Leaf Formation Rate and Mimics Shoot Meristem Integrity Defects Associated with AMP1 Deficiency.
Specimen part, Treatment
View SamplesAffymetrix Mouse Gene 1.0 ST Array profiles were generated from acticular cartilage derived from CBA and Str/ort mice at three ages (8W, 18W, 40W), corresponding to stages prior to, at and late after natural osteoarthritis (OA) onset in OA-prone Str/ort mice.
Time-series transcriptional profiling yields new perspectives on susceptibility to murine osteoarthritis.
Age, Specimen part
View SamplesHere we tested a hypothesis that epileptogenesis influences expression pattern of genes in the basolateral amygdala that are critical for fear conditioning. Whole genome molecular profiling of basolateral rat amygdala was performed to compare the transcriptome changes underlying fear learning in epileptogenic and control animals. Our analysis revealed that after acquisition of fear conditioning 26 genes were regulated differently in the basolateral amygdala of both groups. Thus, our study provides the first evidence that not only the damage to the neuronal pathways but also altered composition or activity level of molecular machinery responsible for formation of emotional memories within surviving pathways can contribute to impairment in emotional learning in epileptogenic animals. Understanding the function of those genes in emotional learning provides an attractive avenue for identification of novel drug targets for treatment of emotional disorders after epileptogenesis-inducing insult.
Epileptogenesis alters gene expression pattern in rats subjected to amygdala-dependent emotional learning.
No sample metadata fields
View SamplesMacrophages, dendritic cells, conventional CD4+ T cells, CD8+ T cells, and regulatory T cells isolated from mouse colon cancer model MC38 tumors implanted subcutaneously to young (3 month) and aged (12 month) mice were sequenced using ImmGen's standard ultra-low input RNA-seq pipeline, in order to study age-dependent differences in intraltumoral immune cell functions and their impact on tumor control Overall design: Samples collected at the Center for Systems Biology at Mass General Hospital, shipped frozen to a central location, and sequenced using ImmGen's standard RNA-seq pipeline
Age-related tumor growth in mice is related to integrin α 4 in CD8+ T cells.
Age, Specimen part, Cell line, Subject
View SamplesTBI was induced with lateral fluid-percussion injury in adult male rats. Genome-wide RNA-seq of the perilesional cortex, ipsilateral thalamus and dorsal hippocampus was performed at 3 months post-TBI. The data highlighted chronic transcriptional changes, particularly, in the perilesional cortex and thalamus. Genes showing a significantly altered expression both in the cortex and thalamus were submitted to the LINCS web query to identify novel pharmacotherapies to improve post-TBI outcome. Overall design: TBI was induced to 5 rats, 5 sham operated served as a controls.
Analysis of Post-Traumatic Brain Injury Gene Expression Signature Reveals Tubulins, Nfe2l2, Nfkb, Cd44, and S100a4 as Treatment Targets.
No sample metadata fields
View SamplesPoorly differentiated thyroid carcinomas (PDTC) represent a heterogeneous, aggressive entity, presenting features that suggest a progression from well-differentiated carcinomas.
Gene expression profiling associated with the progression to poorly differentiated thyroid carcinomas.
Sex, Age, Specimen part
View SamplesOBJECTIVE: To analyze genome-wide changes in chondrocyte gene expression in a surgically induced model of early osteoarthritis (OA) in rats, to assess the similarity of this model to human OA, and to identify genes and mechanisms leading to OA pathogenesis. METHODS: OA was surgically induced in 5 rats by anterior cruciate ligament transection and partial medial meniscectomy. Sham surgery was performed in 5 additional animals, which were used as controls. Both groups underwent 4 weeks of forced mobilization, 3 times per week. RNA was extracted directly from articular chondrocytes in the OA (operated), contralateral, and sham-operated knees. Affymetrix GeneChip expression arrays were used to assess genome-wide changes in gene expression. Expression patterns of selected dysregulated genes, including Col2a1, Mmp13, Adamts5, Ctsc, Ptges, and Cxcr4, were validated by real-time polymerase chain reaction, immunofluorescence, or immunohistochemistry 2, 4, and 8 weeks after surgery. RESULTS: After normalization, comparison of OA and sham-operated samples showed 1,619 differentially expressed probe sets with changes in their levels of expression >/=1.5-fold, 722 with changes >/=2-fold, 135 with changes >/=4-fold, and 20 with changes of 8-fold. Dysregulated genes known to be involved in human OA included Mmp13, Adamts5, and Ptgs2, among others. Several dysregulated genes (e.g., Reln, Phex, and Ltbp2) had been identified in our earlier microarray study of hypertrophic chondrocyte differentiation. Other genes involved in cytokine and chemokine signaling, including Cxcr4 and Ccl2, were identified. Changes in gene expression were also observed in the contralateral knee, validating the sham operation as the appropriate control. CONCLUSION: Our results demonstrate that the animal model mimics gene expression changes seen in human OA, supporting the relevance of newly identified genes and pathways to early human OA. We propose new avenues for OA pathogenesis research and potential targets for novel OA treatments, including cathepsins and cytokine, chemokine, and growth factor signaling pathways, in addition to factors controlling the progression of chondrocyte differentiation.
Global analyses of gene expression in early experimental osteoarthritis.
No sample metadata fields
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