Mir100

RNAcentral ID: URS000075B831_10090
Organism: Mus musculus
Review Status: COMPLETE
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Gene Description

Mir100 encodes the mouse mir-100 precursor. Its mature product is a guide RNA directing Argonaute/RISC to complementary sites in target mRNAs. Its best-supported specific role is in embryonic stem cell differentiation, where miR-100 represses the chromatin remodeller Smarca5 and is required for proper differentiation. mir-100 is abundant and broadly expressed, so it recurs in many miRNA profiling surveys; those appearances are a consequence of its abundance rather than evidence of participation in the processes surveyed.

Existing Annotations Review

GO Term Evidence Action Reason
GO:0016442 RISC complex
IEA
GO_REF:0000115
ACCEPT
Summary: Rfam2GO annotation placing the mature miRNA in RISC.
Reason: Mature miR-100 is loaded into Argonaute/RISC; this is core to how the gene product works.
GO:0035195 miRNA-mediated post-transcriptional gene silencing
IEA
GO_REF:0000115
ACCEPT
Summary: Rfam2GO annotation of the generic microRNA process.
Reason: Correct and core for a mir-100 precursor.
GO:0035195 miRNA-mediated post-transcriptional gene silencing
IDA
PMID:20439489
miRNA 34a, 100, and 137 modulate differentiation of mouse em...
ACCEPT
Summary: Direct-assay support for miR-100-mediated repression of Smarca5.
Reason: Smarca5 was shown to be a direct target of miR-100, which is post-transcriptional silencing by the mature miRNA.
Supporting Evidence:
PMID:20439489
we first demonstrated that Smarca5 is a direct target of miR-100
GO:2000738 positive regulation of stem cell differentiation
IMP
PMID:20439489
miRNA 34a, 100, and 137 modulate differentiation of mouse em...
ACCEPT
Summary: The functionally validated role from this paper, established by anti-miR suppression and overexpression.
Reason: miR-100 is one of the three miRNAs the study tested rather than merely profiled: suppression by anti-miRs blocked ESC differentiation and overexpression altered differentiation markers. This is the correct representation of what the paper shows about mir-100, and it is the reason the LIF row below is redundant as well as unsupported.
Supporting Evidence:
PMID:20439489
These results demonstrate that miR-34a, miR-100, and miR-137 are required for proper differentiation of mouse ESCs
PMID:20439489
The suppression of these three miRNAs by anti-miRs caused the block of ESC differentiation induced by LIF withdrawal
GO:1990830 cellular response to leukemia inhibitory factor
IEP
PMID:20439489
miRNA 34a, 100, and 137 modulate differentiation of mouse em...
MARK AS OVER ANNOTATED
Summary: Batch expression row from the same paper whose validated finding is already captured by the IMP annotation above; the term also misdescribes the experiment.
Reason: This row and the IMP row above come from the same paper, and the contrast is the point. The IMP row records what was demonstrated - miR-100 is required for ESC differentiation via Smarca5. This IEP row is one of 291 annotations to a single term generated from the same study's expression survey. The term is also a poor description of the experiment: LIF was withdrawn to induce differentiation, so the miRNAs went up in the absence of LIF, which is not a cellular response to LIF. Even for a miRNA the paper did validate, the batch row adds a wrong term rather than support.
Supporting Evidence:
PMID:20439489
The suppression of these three miRNAs by anti-miRs caused the block of ESC differentiation induced by LIF withdrawal
GO:0007605 sensory perception of sound
IEP
PMID:23646144
Identifying microRNAs involved in degeneration of the organ ...
REMOVE
Summary: Derived from an ageing expression survey that never names mir-100, and pointed at normal hearing when the study is about its loss.
Reason: Two independent problems. First, the PMC full text of the cited paper contains no mention of miR-100, so the annotation comes from a supplementary microarray table listing miRNAs whose abundance shifted with age; nothing connects mir-100 to auditory function. Second, the study is about degeneration of the organ of Corti during age-related hearing loss, and its own conclusion is explicitly correlative - expression changes precede functional change. Annotating mir-100 as acting upstream of or within the normal process of sound perception inverts what was measured. One of 100 IEP rows to this term from this paper.
Supporting Evidence:
PMID:23646144
Our study suggests that changes in miRNA expression precede morphological and functional changes
PMID:23646144
We showed that 111 and 71 miRNAs exhibited differential expression in the C57 and CBA mice, respectively
GO:0060291 long-term synaptic potentiation
IEP
PMID:25858512
miR-26a and miR-384-5p are required for LTP maintenance and ...
REMOVE
Summary: mir-100 is not discussed anywhere in the cited paper; the row reflects membership of the detected-miRNA set.
Reason: The bottom tier of the 130-member IEP batch from this study. The paper detected 372 miRNAs, found 12 that changed, and functionally validated three; miR-100 is in none of those groups and the PMC full text does not mention it. The only fact behind this annotation is that mir-100 was present at detectable levels in hippocampal slices, which is true of hundreds of miRNAs and says nothing about LTP.
Supporting Evidence:
PMID:25858512
Of the 12 miRNAs changed in LTP, 6 were down- and 6 were upregulated
PMID:25858512
we identified 372 miRNAs
GO:0045202 synapse
IDA
PMID:22897173
Primary microRNA precursor transcripts are localized at post...
KEEP AS NON CORE
Summary: Localization of pri-miRNA transcripts to post-synaptic densities.
Reason: The cited study directly assays pri-miRNA localization at post-synaptic densities in adult mouse forebrain, which supports a synaptic location. Kept as non-core because localization is not the activity that defines mir-100.
GO:0071475 cellular hyperosmotic salinity response
IDA
PMID:17028171
miR-7b, a microRNA up-regulated in the hypothalamus after ch...
UNDECIDED
Summary: Cannot be adjudicated; the cached full text does not mention mir-100.
Reason: PMC full text is cached for this reference and contains no mention of miR-100; the paper concerns miR-7b inhibiting Fos translation after hyperosmolar stimulation. Because the cached text may be incomplete and the curator saw the published figures, this is left undecided rather than removed.
GO:0042552 myelination
IDA
PMID:20805985
Ablation of Dicer from murine Schwann cells increases their ...
KEEP AS NON CORE
Summary: Retained on the curator's authority; the cited paper does discuss miR-100.
Reason: Unlike several other references on this gene, the cached full text of this Dicer-ablation study does mention miR-100, so the curator had direct material. Kept as non-core because a Schwann-cell myelination phenotype from global Dicer loss is a pathway-level context rather than a demonstrated mir-100 activity.

Core Functions

miRNA guide activity directing Argonaute/RISC to target mRNAs, used in embryonic stem cells to repress the chromatin remodeller Smarca5 and permit differentiation

Supporting Evidence:
  • PMID:20439489
    we first demonstrated that Smarca5 is a direct target of miR-100

References

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Suggested Questions for Experts

Q: Does mir-100 have any role in the auditory or synaptic processes it is currently annotated to, or are those annotations purely a consequence of its abundance in profiling studies?

Suggested experts: microRNA biologists, auditory neuroscientists

Q: Which mir-100 targets besides Smarca5 mediate its effect on stem cell differentiation?

Suggested experts: stem cell biologists

Suggested Experiments

Experiment: Conditional mir-100 deletion in the inner ear with auditory brainstem response measurement across ageing

Hypothesis: Loss of mir-100 does not alter hearing thresholds, confirming that the ageing-survey annotation reflects correlation rather than function

Type: mouse genetics

Experiment: Ago CLIP in embryonic stem cells during LIF withdrawal, comparing wild-type and mir-100-null cells

Hypothesis: Smarca5 is one of a small set of mir-100-dependent targets that change Argonaute occupancy during differentiation

Type: high-throughput sequencing

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