Evidence card: NCBI:GeneID:136275927

Real public-study evidence. Association evidence only; not a validated biomarker.

How to interpret expression as evidence for resilience. Differential expression alone does not establish a resilience marker; higher expression does not necessarily mean greater resilience.

This feature was selected among up to ten displayed findings in at least one study. All available rows for it are shown below, including nonsignificant and exploratory results. Presence in multiple datasets does not establish independent replication: exposures, tissues, life stages, and phenotype meanings differ. No cross-study score or pooled effect is calculated.

Guide to effect sizes, uncertainty and gene descriptions.

Study-specific effects

Study / design	RefSeq description	Contrast	Effect scale	Effect	Standard error	Adjusted p-value	Interpretation
PRJEB86646	uncharacterized LOC136275927	30C_vs_23C_fed_before_oshv1	log2 fold change	0.383	1.08	0.8252	Study-level association; see design caveats
PRJNA735889	uncharacterized LOC136275927	ph_6.5_6.8_vs_ph_7.4_7.8_23d_juveniles	log2 fold change	-6.765	1.037	2.427e-08 (nominal only)	Exploratory; tank clustering unmodeled
PRJEB86618	uncharacterized LOC136275927	starved_vs_fed_ad_libitum_16d_before_oshv1	log2 fold change	2.57	1.689	0.2082	Study-level association; see design caveats

CGIG_HEAT_RNASEQ_PRJEB86646

Phenotype interpretation: Lower mortality after OsHV-1 mu-Var cohabitation is favorable. The publication reports that 30 C limits POMS development and improves survival, through metabolic reprogramming and stronger baseline and induced antiviral immunity. AREE records the whole-spat transcriptional state at 30 C before infection, not survival per library.

Biological replication: 12 RNA-seq libraries, all sampled at 0 h post-cohabitation: 6 at 23 C and 6 at 30 C, three per temperature in each of the two families. Each library pools the soft tissue of 10 live spat taken from one tank, as in the DECICOMP starvation arm.

Evidence classification: resilience_associated. Tissue: whole_soft_tissue; life stage: spat.

Quality flags: raw_reanalysis;temperature_response;pre_infection_baseline;family_blocked_contrast;shared_control_group_with_PRJEB86618;dependence_group=DECICOMP_PRJEB86525_0h_controls.

Study limitations:

The six 23 C fed control libraries (PRJEB86525, 0 h) are the same libraries used as controls in CGIG_STARVATION_RNASEQ_PRJEB86618. The two harmonized studies therefore share a reference group, so their effect estimates are correlated and must not be treated as independent in a meta-analysis.
The contrast uses only the 0 h libraries, sampled when the OsHV-1 mu-Var donors were added, so it captures temperature without infection. The 36 later libraries (3-72 h) follow infection, which progresses far less at 30 C, and are not used.
Each tank held both families, so the F11N and F14R libraries with the same replicate number probably share a tank. The model ~ family + condition treats the six libraries per temperature as independent, although only three tanks per temperature are independent units.
The 30 C arm and the 23 C controls were held in separate tanks of one experiment at the Argenton station, so tank is nested in temperature.
Condition, family, time and replicate come from the ENA sample aliases and titles (sam_P_<3 fed 23 C | 4 fed 30 C>_), and the two sources agree for every library.
The publication reports enhanced baseline antiviral immunity at 30 C. At 0 h this reanalysis finds the opposite for several classic antiviral markers: all 13 significant interferon-induced protein 44 genes, 10 of 12 significant tumor necrosis factor genes and both significant 2’-5’-oligoadenylate synthetase genes are lower at 30 C. The publication is not open access and its gene lists were not compared, so whether this reflects different gene sets, a different time point or a real disagreement is unresolved.
Pools at 30 C map about three points less to the transcriptome than pools at 23 C. The shift is systematic but small beside the expression effects.

Provenance: Reference GCF_963853765.1 / RS_2024_06; mapping exact; workflow 0.1.0.

Harmonized evidence. Processed input. Input SHA-256: abbc33a2dc6e48a0f0a903bbca1d4bce3f90c56927e80ff5c5bc3e88dd6c0c5c.

CGIG_OA_RNASEQ_PRJNA735889

Phenotype interpretation: Lutier et al. report physiological tipping points at pHT 7.3-6.9 that coincide with a major reshuffling of the transcriptome and membrane lipids; AREE records the whole-animal transcriptional response below the tipping window relative to above it, not a measured tolerance phenotype

Biological replication: 50 oysters, one whole-animal library each: 25 control and 25 acidified, 5 per tank. A 51st library, 13Ebis, is a resequencing of oyster 13E and is not analysed. Each pH level is one tank, so oysters are replicates within tank and the 10 tanks are the replicates of the pH contrast.

Evidence classification: environmental_exposure. Tissue: whole_organism; life stage: juvenile.

Quality flags: raw_reanalysis;ocean_acidification_response;ph_band_contrast_tipping_window_excluded;no_ambient_ph_reference;one_tank_per_ph_level;gametogenesis_blocked_contrast;fdr_lt_0.05;exploratory_tank_clustering_unmodeled.

Exploratory uncertainty: Tank clustering is unmodeled. Standard errors and adjusted p-values above are nominal only; this row is excluded from pooling and significance rewards.

Study limitations:

The study is a 15-level pH gradient (pHT 6.5-7.8, 76 libraries). AREE reduces it to a two-group contrast at the authors’ tipping-point window: the five tanks inside pHT 7.3-6.9 (tanks 1, 6, 4, 11 and 10; 25 libraries) are excluded and not downloaded. Effect sizes are therefore log2 fold changes between two pH bands, not slopes per pH unit, and they mix the response across five pH levels on each side.
There is no ambient-pH tank; the reference band (pHT 7.4-7.8) is itself below present-day coastal pH, so the contrast understates the full response to acidification.
Each pH level is a single tank, so tank and pH are confounded at the level of a single pH; with five tanks per band the band contrast has tank-level replication, but DESeq2 treats the 50 analysed oysters as independent and does not model tank. Standard errors, p-values and FDR values are exploratory and may overstate precision. A tank-aware reanalysis is required before inferential use; PCA and per-tank residual checks do not correct the error model.
Tank 15 is labelled ‘pHT 6.5 bis’ in BioSample: a second tank at pHT 6.5 alongside tank 9.
Library 13Ebis (SRR14803132) has a different index from 13E (SRR14803133) and about half its reads. The expressed-SNP check shows it is the same oyster (allele-frequency difference 0.026, below the 0.032 expected for one RNA resequenced; the next closest pair differs by 0.198), so it is kept in the manifest but left out of the analysis.
Male gametogenesis is unbalanced between bands: a spermatogenesis module is active in 11 of 25 control and 2 of 25 acidified oysters (Fisher p = 0.008), spread across all five control tanks, which suggests that low pH delays or suppresses the onset of spermatogenesis in 5-month-old juveniles. The primary model blocks on this call (~ gametogenesis + condition) so the evidence records a gametogenesis-adjusted association with pH, without establishing a direct causal response; the unadjusted model is kept as a sensitivity analysis. The call is a transcriptional proxy derived from the same data (scripts/score_prjna735889_gametogenesis.py), not a histological sex or maturation call, and with only two active acidified oysters the gametogenesis effect is estimated mostly from the control band.
Condition, tank and pH come from the NCBI BioSample title, treatment and growth_protocol attributes; every library is paired-end. ENA served the FASTQs at about 80 KB/s on 2026-10-02, so all 51 runs are taken from the NCBI Open Data mirror as .sra archives checked against the size and MD5 NCBI publishes (CGIG_OA_RNASEQ_PRJNA735889_sra_locations.tsv), and each converted FASTQ pair must match the manifest read count.

Provenance: Reference GCF_963853765.1 / RS_2024_06; mapping exact; workflow 0.1.0.

Harmonized evidence. Processed input. Input SHA-256: a8f7485ec9436cc334d22b6819d7137f37dccb753fa688700c49d264cb7c0dda.

CGIG_STARVATION_RNASEQ_PRJEB86618

Phenotype interpretation: Lower mortality after OsHV-1 mu-Var cohabitation is favorable. Starved spat had lower final mortality than fed spat (F14R 34.8% versus 75.5%; F11N 93.3% versus 100%; log-rank p < 0.05 in both families), and deaths began later (120 h versus 72-96 h post-cohabitation). AREE records the whole-spat transcriptional state produced by starvation before infection, not survival per library.

Biological replication: 12 RNA-seq libraries used for the contrast, all sampled at 0 h post-cohabitation: 6 fed and 6 starved, three per diet in each of the two families. Each library pools the soft tissue of 10 live spat taken from one tank. The experiment used three tanks per diet, and each tank held both families.

Evidence classification: resilience_associated. Tissue: whole_soft_tissue; life stage: spat.

Quality flags: raw_reanalysis;nutritional_limitation_response;pre_infection_baseline;family_blocked_contrast;dependence_group=DECICOMP_PRJEB86525_0h_controls.

Study limitations:

The contrast uses only the 0 h libraries. They were sampled when the OsHV-1 mu-Var donor oysters were added, so they capture starvation without infection. The other 71 deposited libraries (3-72 h) follow each diet through infection, when the fed spat carry far more virus. A diet effect pooled across that time course would mix starvation with differential infection progression, so they are not used here.
Each tank held both families, so the F11N and F14R libraries with the same replicate number probably share a tank. The public metadata do not state that replicate numbers correspond to tanks. The model ~ family + condition treats the six libraries per diet as independent, although only three tanks per diet are independent units, so the error model may be somewhat optimistic.
The two families differ strongly in POMS susceptibility and in how much starvation protected them, so a single diet effect averaged over both may hide family-specific responses.
The ENA sample titles call every time point ‘hours post-infection’, including 0 h. The publication shows the 0 h pools were sampled at the start of cohabitation, before viral DNA load rose.
The publication reports 84 sequenced libraries and 83 are deposited; the starved F14R 6 h replicate 3 is absent. It also excluded one F11N 48 h replicate 2 library with 21% mapping without naming its diet, and both such libraries are deposited. Neither affects the 0 h contrast.
The STAR Methods key-resources table swaps the two RNA-seq accessions (PRJEB86618 ‘for the Fed condition’). The data statement, the ENA study titles and every ENA sample title agree that PRJEB86618 is the starved arm and PRJEB86525 the fed arm, and the manifest follows them.
Condition, family, time and replicate come from the ENA sample aliases and titles (sam_P_<3 fed | 5 starved>_), and the two sources agree for every library.
The publication aligned reads with STAR to the Penaloza et al. 2021 assembly and analysed the 0 h diet contrast with WGCNA, treating the families as replicates, not with a per-gene differential expression test. Supplementary Table S5 lists the 13,238 genes in the three diet-associated modules (6,307 in the fed-associated turquoise module; 3,603 blue and 3,328 brown starved-associated), with module membership scores and, for 9,540 of them, an NCBI GeneID. It supports a direction-level comparison but gives no effect sizes or per-gene significance.
The DECICOMP 30 C fed arm (PRJEB86646) shares the same families, design and fed controls, but the publication does not use it and it is outside this record.
Against publication Supplementary Table S5, 8,609 genes of the diet-associated WGCNA modules have a GeneID tested here. 98.3% of fed-module genes are lower and 97.5% of starved-module genes are higher in starved pools (99.0% among genes with |module membership| > 0.8), and only 37 are significant in the opposite direction.
Nearly half the tested genes are significant because the design has low within-cell variance (pools of 10 full sibs, BCV 9.8%) and 16 days of starvation is a large perturbation. The replicate genotype check rules out resequenced RNA. Pooling still removes individual variation, so the error model describes pool-to-pool variation, not animal-to-animal variation.
Starved pools map about two points less to the transcriptome and more to the genome decoy than fed pools. The shift is small beside the expression effects but systematic, and it may reflect more unspliced or intronic RNA under starvation.

Provenance: Reference GCF_963853765.1 / RS_2024_06; mapping exact; workflow 0.1.0.

Harmonized evidence. Processed input. Input SHA-256: 7f2cdd37eb935232ae95a393eae8b8fd6fc09a04313c6127ab75f9d0422d0d57.

Next validation step

Independent biological replication with matched exposure and measured phenotype, an appropriate experimental-unit model, and targeted validation in the relevant tissue and life stage.