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TJ411(fer-15(b26)II; age-1(hx542)II) vs. BA713(fer-15(b26)II)

ABSTRACT: To identify changes in gene expression in age-1 mutants, we compared expression in fer-15(b26) animals to expression in fer-15(b26); age-1(hx542) mutants. We prepared RNA from young adult fer-15(b26) mutants grown at 25?C (five samples prepared at Stanford University and six samples prepared at the University of Colorado) and young adult fer-15(b26); age-1(hx542) mutants (four samples at Stanford University and six samples at the University of Colorado). Set of arrays that are part of repeated experiments Place of growth: Stanford vs Colorado Genotype: mutant strains vs wt (N2) mixed stage; some expts are reverse dye

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE12166 | GEO | 2008/07/29

SECONDARY ACCESSION(S): PRJNA114319

REPOSITORIES: GEO

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TJ411(fer-15(b26)II; age-1(hx542)II) vs. BA713(fer-15(b26)II)

Project description:To identify changes in gene expression in age-1 mutants, we compared expression in fer-15(b26) animals to expression in fer-15(b26); age-1(hx542) mutants. We prepared RNA from young adult fer-15(b26) mutants grown at 25?C (five samples prepared at Stanford University and six samples prepared at the University of Colorado) and young adult fer-15(b26); age-1(hx542) mutants (four samples at Stanford University and six samples at the University of Colorado). Set of arrays that are part of repeated experiments Place of growth: Stanford vs Colorado Genotype: mutant strains vs wt (N2) mixed stage; some expts are reverse dye Biological Replicate Computed

2008-07-29 | E-GEOD-12166 | biostudies-arrayexpress

TJ1081)fer-15(b26)II; daf-16(m26)I) vs. BA713(fer-15(b26)II)

Project description:To identify changes in gene expression in daf-16 mutants, we compared expression in fer-15 young adults to expression in fer-15(b26); daf-16(m26) young adults grown at 25?C. At Stanford University, four samples of fer-15 and five samples of fer-15; daf-16 animals were prepared. At the University of Colorado, seven samples of fer-15 and six samples of fer-15; daf-16 was prepared. Set of arrays that are part of repeated experiments Place of growth: At Stanford vs Colorado Genotype: mutant strains vs wt (N2) mixed stage; some expts are reverse dye (wt in channel 2)

2008-07-29 | GSE12167 | GEO

TJ1081)fer-15(b26)II; daf-16(m26)I) vs. BA713(fer-15(b26)II)

2008-07-29 | E-GEOD-12167 | biostudies-arrayexpress

C. elegans fer-1 mutant gene expression profile

2009-06-25 | GSE16753 | GEO

Transcription profiling of muscle from wild type and fer-1 mutant C. elegans

Project description:In vertebrate muscle, loss of Dysferlin results in the activation of compensatory muscle gene expression, even at pre-pathological stages. We hypothesized that if C. elegans fer-1 is also expressed in muscle, then fer-1 mutant worms might also exhibit compensatory muscle gene expression. To test this hypothesis, we used Affymetrix microarrays to profile gene expression from synchronized wild type and fer-1 mutant adults. To improve the specificity of this approach, we profiled two well characterized loss-of-function fer-1 mutants (hc1ts and hc24ts) and considered genes that changed similarly in both mutants as fer-1-regulated transcripts. Experiment Overall Design: For each genotype, six individual replicates were performed and were hybridized to Affymetrix C. elegans Genechips using the manufacturerâs recommended protocols. The best four preparations (as determined by the overall Pearson Correlation within a genotype) were used for RNA labeling and hybridization.

2009-07-05 | E-GEOD-16753 | biostudies-arrayexpress

The LRX-RALF-FER cell wall integrity sensing module controls plant growth and salt stress responses by modulating multiple plant hormones

Project description:Plants have evolved cell wall integrity signaling pathways to maintain cell wall homeostasis during rapid growth and in response to environmental stress. The cell wall leucine-rich repeat extensins LRX3/4/5, the RAPID ALKALINIZATION FACTOR (RALF) peptides RALF22/23, and FERONIA (FER) function as a module to regulate plant growth and salt stress responses via the sense of cell wall integrity. However, the intracellular signaling pathways that mediate the effects of the LRX3/4/5-RALF22/23-FER module are still largely unknown. Here, we report that jasmonic acid (JA), salicylic acid (SA), and abscisic acid (ABA) accumulate constitutively in lrx345 and fer mutants. Blocking JA pathway rescues the retarded growth phenotype of the lrx345 and fer-4 mutants, while disruption of ABA biosynthesis suppresses the salt-hypersensitivity of these mutants. Many salt stress-responsive genes display abnormal expression patterns in the lrx345 and fer-4 mutants, as well as in wild type plants treated with epigallocatechin gallate (EGCG), an inhibitor of pectin methylesterases, suggesting that the cell wall integrity is a critical factor that determines the expression of stress-responsive genes. Production of reactive oxygen species (ROS) is constitutively increased in the lrx345 and fer-4 mutants, and inhibition of ROS accumulation suppresses the salt-hypersensitivity of these mutants. Together, our results suggest that the LRX3/4/5-RALF22/23-FER module controls plant growth and salt stress responses by regulating hormonal homeostasis and ROS accumulation.

2021-07-15 | GSE136268 | GEO

Transcription profiling of long-lived C.elegans daf-2 pathway mutants with wild type/short-lived mutants

Project description:Comparison of long-lived daf-2 pathway mutants with wild type/short-lived mutants. A: age-1 fer-15; fem-1 vs. fer-15; fem-1. B: age-1 fer-15; fem-1 vs. fer-15; fem-1. C: fer-15; daf-2(mu150); fem-1 vs. fer-15; fem-1. D: fer-15; daf-2(mu150); fem-1 vs. fer-15; fem-1. E: daf-16::gfp in daf-16(mu86);daf-2(e1370) vs. daf-16(mu86);daf-2(e1370). F: daf-2(e1368); fer-15; fem-1 vs. fer-15; fem-1. G: fer-15; daf-2(mu150); fem-1 vs. fer-15; fem-1. H: age-1 fer-15; fem-1 vs. fer-15; fem-1. I: fer-15; daf-2(mu150); fem-1 vs. fer-15; fem-1. J: daf-16::gfp in daf-2(e1370); daf-16(mu86) vs. daf-2(e1370); daf-16(mu86). K: daf-2(mu150) vs. wild type. L: daf-2(e1370) vs. daf-2(e1370); daf-16(mu86). M: daf-2(e1370) vs. daf-2(e1370); daf-16(mu86). N: daf-2(e1370) vs. daf-2(e1370); daf-16(mu86).

2003-07-17 | E-MEXP-7 | biostudies-arrayexpress

Transcriptome analysis of gene expression changes in fer-8 and the parental line

Project description:To reveal transcriptional changes in the fer-8 mutant that could explain the increase in Pseudomonas colonization, we performed transcriptional profiling in both shoots and roots from fer-8 and the parental line. We identified 675 up-regulated genes in the shoots of fer-8 relative to wildtype plants. Surprisingly, we found only 82 up-regulated genes in fer-8 roots relative to the parental line, and there were no significantly enriched GO terms. In contrast, we found that the genes upregulated in shoots were enriched in GO terms related to defense, response to fungi, and JA signaling, consistent with previous reports of JA activation in the shoots of another fer mutant fer-4.

2021-04-21 | GSE167143 | GEO

FER-regulated genes under moderate intensity light

Project description:Col-0 and fer-4 seedlings grown for 7 d under moderate intensity light (150 PFD) were used for RNA-sequencing

2021-04-20 | GSE172298 | GEO

FER kinase governs invasive tumor growth through dynamic control of oncogenic growth factor receptor activity

Project description:EGFR antagonism using monoclonal antibodies remains the only approved and targeted first line treatment option for non-resectable head and neck squamous cell carcinoma (HNSCC), yielding a modest 13% response rate. While it is clear that alternative growth factor receptor (GFR) signals govern refractory behavior towards EGFR antagonism, it remains unknown which upstream mechanisms control subcellular GFR activation. Here, we show that FER, a non-receptor tyrosine kinase, controls invasive tumor growth through dynamic GFR activation and recycling. Using patient derived organoid (PDO) models HNSCC we demonstrate that FER is essential for invasive growth in collagen extracellular matrix (ECM) networks. We show that inactivation of FER impairs growth factor dependent phosphorylation of EGFR-Y1068 and MET-Y1234/5. Additionally, FER controls ligand dependent endocytic recycling, and endocytic velocity, implying multifactorial functional regulation of proximal receptors during HNSCC invasion. Loss of function experiments using either genetic intervention or a FER PROteolysis-TArgeting Chimera (PROTAC) strategy in PDO-based xenograft mouse models, demonstrate that FER is essential for invasive growth and metastasis of HNSCC. Finally, we demonstrate direct clinical relevance by showing that FER expression levels correlate with poor survival in HNSCC patients. In sum, we conclude that FER is a master regulator of HNSCC invasive growth and metastasis, and nominate FER as a prominent candidate for targeted clinical intervention in HNSCC patients.

2024-03-31 | GSE255878 | GEO

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