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Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4

ABSTRACT: To find genes downstream of the TGF-beta Sma/Mab pathway associated with body size regulation in C. elegans.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE23448 | GEO | 2010/09/01

SECONDARY ACCESSION(S): PRJNA133339

REPOSITORIES: GEO

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Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4

Project description:To find genes downstream of the TGF-beta Sma/Mab pathway associated with body size regulation in C. elegans. Three replicates comparing RNA from sma-2(e502) L4 whole animal with RNA from wild-type L4 whole animal, in which one is dye flipped. Plus one array comparing RNA from sma-4(e729) L4 whole animal with RNA from wild-type L4 whole animal.

2010-09-01 | E-GEOD-23448 | biostudies-arrayexpress

TGF-beta Sma/Mab signaling regulates a set of genes in oocytes associated with reproductive aging and another set in L4 associated with body size growth

Project description:Reproductive cessation is perhaps the earliest aging phenotypes humans experience. Similarly, C. elegans' reproduction ceases in mid-adulthood. Although somatic aging has been studied in both worms and humans, mechanisms regulating reproductive aging are not yet understood. Here we show that TGF-beta Sma/Mab activity regulates reproductive aging transcriptionally separable from its regulation of body size growth. This SuperSeries is composed of the following subset Series: GSE23446: Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte GSE23447: Reproductive aging: fem-1 day 3 oocyte vs fem-1 day 8 oocyte GSE23448: Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4 Refer to individual Series

2010-09-01 | E-GEOD-23509 | biostudies-arrayexpress

TGF-beta Sma/Mab signaling regulates a set of genes in oocytes associated with reproductive aging and another set in L4 associated with body size growth

2010-09-01 | GSE23509 | GEO

Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte

Project description:To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging.

2010-09-01 | GSE23446 | GEO

Reproductive aging: sma-2;fem-1 day 8 oocyte vs fem-1 day 8 oocyte

Project description:To find genes downstream of the TGF-beta Sma/Mab pathway in C. elegans oocytes associated with reproductive aging. Eight replicates comparing RNA from oocyte samples collected from day 8 sma-2(e502);fem-1(hc17) animals with RNA from oocyte samples collected from day 8 fem-1(hc17) animals. Five out of eight are dye-flipped.

2010-09-01 | E-GEOD-23446 | biostudies-arrayexpress

TGF-beta Sma/Mab signaling mutations uncouple reproductive aging from somatic aging.

Project description:Female reproductive cessation is one of the earliest age-related declines humans experience, occurring in mid-adulthood. Similarly, Caenorhabditis elegans' reproductive span is short relative to its total life span, with reproduction ceasing about a third into its 15-20 day adulthood. All of the known mutations and treatments that extend C. elegans' reproductive period also regulate longevity, suggesting that reproductive span is normally linked to life span. C. elegans has two canonical TGF-beta signaling pathways. We recently found that the TGF-beta Dauer pathway regulates longevity through the Insulin/IGF-1 Signaling (IIS) pathway; here we show that this pathway has a moderate effect on reproductive span. By contrast, TGF-beta Sma/Mab signaling mutants exhibit a substantially extended reproductive period, more than doubling reproductive span in some cases. Sma/Mab mutations extend reproductive span disproportionately to life span and act independently of known regulators of somatic aging, such as Insulin/IGF-1 Signaling and Dietary Restriction. This is the first discovery of a pathway that regulates reproductive span independently of longevity and the first identification of the TGF-beta Sma/Mab pathway as a regulator of reproductive aging. Our results suggest that longevity and reproductive span regulation can be uncoupled, although they appear to normally be linked through regulatory pathways.

| S-EPMC2791159 | biostudies-literature

Caenorhabditis elegans

Project description:Body size regulation and TGF-beta Sma/Mab pathway: sma L4 vs N2 L4

| PRJNA133339 | ENA

Gene expression profile of sma-3 mutant Caenorhabditis elegans

Project description:N2 (wildtype) control animals vs. sma-3 mutants vs. sma-6 mutants; 5 replicates each.

2022-02-18 | GSE151035 | GEO

SMA-10 Is a Non-Canonical Member of the TGF-β Sma/Mab Pathway and Immunity Regulator via the DAF-2 Insulin Receptor in Caenorhabditis elegans.

Project description:Transforming growth factor β (TGF-β) signalling pathways are highly conserved across metazoa and play essential roles not only during development but also in adult tissue maintenance. Alterations of these pathways usually result in a plethora of pathologies. In the nematode Caenorhabditis elegans, the TGF-β Sma/Mab (small/male abnormal) pathway regulates various worm phenotypes such as body size, immune response, ageing, matricide and reproductive span. SMA-10 has been described as a positive modulator of worm body size through the TGF-β Sma/Mab pathway. To better understand if SMA-10 is a core component of the pathway, we use gene epistatic analysis to assess the contribution of SMA-10 to various phenotypes regulated by TGF-β Sma/Mab. We confirm that SMA-10 controls body size and find that it also affects the matricide and reproductive span of the nematodes. However, neither male tail formation (previously reported) nor ageing appeared altered. Lastly, although null sma-10 worms are more susceptible to Pseudomonas aeruginosa infections than wild-types, this response does not depend on TGF-β Sma/Mab but on the insulin receptor DAF-2. We also show that the expression of sma-10 in either hypodermis or intestine fully rescues the wild-type immune response. Our results contribute to understanding the role of SMA-10 as a context-dependent component of TGF-β Sma/Mab, and reveal a function of SMA-10 in immunity in association to the Insulin/insulin-like growth factor signalling (IIS) pathway.

| S-EPMC7827673 | biostudies-literature

Gene expression profiling in SMA I and III patients

Project description:Proximal spinal muscular atrophy (SMA) is a neurodegenerative disorder associated with mutations of the survival motor neuron gene SMN and characterized by progressive paralysis caused by degeneration of α–motor neurons of the spinal cord. To better understand the effects of SMN gene defect in SMA skeletal muscle tissues we performed a transcriptional analysis of muscle specimens of patient affected by the two extreme forms of SMA: the most severe type I and the mild type III. Patients of both groups had a variable SMN2 copy number that did not correlate with phenotype severity. The two forms of SMA resulted with a distinct expression profile: in SMA III patients the reduced number of modified genes suggests a proximity to normal condition, whereas in SMA I patients there is highly deregulated picture of gene expression. Genes implicated in signal transduction were up regulated in SMA III condition whereas those typical of energy metabolism and muscle contraction were consistently down regulated in severe disease type. Microarray results were validated, and the expression pattern of gene networks involved in atrophy signaling were completed by RQ-PCR. The analysis shows that specific atrophy pathways are involved: IGF/PI3K/Akt and those regulating MNK1-2 (more precisely TNF-α/p38 MAPK and Ras/ERK pathways). The results suggest also a different picture of atrophy pathways in the two forms of SMA. In particular in SMA I muscles, p38 may be the protein synthesis regulator. Moreover SMA III profile appear to be the result of a more complex transcriptome given by the concurrent presence of atrophic and hyperthrophic fibers. This more favorable condition might be due to action of MTOR whose over expression in SMA III could lead to a compensative hypertrophy. Keywords: disease state analysis

2009-06-08 | GSE8359 | GEO

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