Evidence card: NCBI:GeneID:105318673

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	hypothetical protein	30C_vs_23C_fed_before_oshv1	log2 fold change	-0.3002	0.3488	0.5479	Study-level association; see design caveats
PRJNA298285	hypothetical protein	pH7.9_vs_pH8.1_20C_larvae	log2 fold change	0.0002531	0.07416	0.9999	Study-level association; see design caveats
PRJNA735889	hypothetical protein	ph_6.5_6.8_vs_ph_7.4_7.8_23d_juveniles	log2 fold change	-1.506	0.3731	0.001177 (nominal only)	Exploratory; tank clustering unmodeled
PRJNA826964	hypothetical protein	ocean_acidification_vs_ambient_control	log2 fold change	-1.529	0.7315	0.3229	Study-level association; see design caveats
PRJNA1329250	hypothetical protein	oshv1_microvariant_challenge_vs_unchallenged_control	log2 fold change	-0.1738	0.3384	0.7756	Study-level association; see design caveats
CGIG_PESTO_F0_RNASEQ_PRJEB58194	hypothetical protein	pesticide_mixture_0_48hpf_vs_control_F0_gastrula_dlarva	log2 fold change	-1.728	0.2652	4.683e-07	Study-level association; see design caveats
CGIG_PESTO_F1DIRECT_RNASEQ_PRJEB58194	hypothetical protein	pesticide_mixture_TE_vs_TT_F1_gastrula_pediveliger	log2 fold change	0.1565	0.3609	1	Study-level association; see design caveats
PRJEB86618	hypothetical protein	starved_vs_fed_ad_libitum_16d_before_oshv1	log2 fold change	-1.506	0.5019	0.007409	Study-level association; see design caveats
CGIG_VCRASSOSTREAE_RNASEQ_PRJNA515169	hypothetical protein	vibrio_crassostreae_J2_9_vs_mock_injection_8h	log2 fold change	-0.1155	0.8276	not available	Study-level association; see design caveats
CGIG_VTASMANIENSIS_RNASEQ_PRJNA515169	hypothetical protein	vibrio_tasmaniensis_LGP32_vs_mock_injection_8h	log2 fold change	-0.01529	0.8452	not available	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_LARVAL_OA_RNASEQ_PRJNA298285

Phenotype interpretation: No phenotype is deposited and no publication is linked; AREE records the larval transcriptional response averaged over three developmental stages.

Biological replication: 12 whole-larva libraries: 6 ambient and 6 acidified (pH 7.9, 20 C), two per developmental stage. Each library is presumably a pool of many larvae; whether the two libraries per cell are separate cultures or one culture is not recorded and is tested with the expressed-SNP check.

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

Quality flags: raw_reanalysis;larval_development;pooled_libraries;stage_blocked_contrast;shared_control_group;dependence_group=PRJNA298285_ambient_larvae;no_linked_publication;ocean_acidification_response;replicate_culture_independence_unverified.

Study limitations:

• No publication is linked to the BioProject, and searches of PubMed and Europe PMC (including the accessions PRJNA298285 and SRP064660) on 2026-10-07 found none, so there are no published methods, carbonate chemistry, survival data or results to reconcile against.
• The three AREE records from this study (acidified, warmed, acidified + warmed) test against the same six ambient libraries, so they carry the dependence group PRJNA298285_ambient_larvae and count as one replication group.
• There are two libraries per stage and treatment. The stage block (~ stage + condition) treats them as replicates; whether they come from separate cultures is not recorded and is checked with scripts/check_replicate_genotypes.py.
• The treatments are mild (pH 7.9 against 8.1; 22 C against 20 C), so small transcriptional effects are expected.
• Treatment, stage and replicate come from the ENA sample aliases (C.gigas_) and library names (<Trc | Vg1 | Vg2>_<ambi | acid | warm | intr><A | B>), and agree with the BioSample pH, temperature, dev_stage and age attributes. One library name is a file name (C3759_TAGCTT_L003_R1_001.fastq.gz, late-veliger warmed); it is taken as replicate B because the other late-veliger warmed library is C3752_Vg2_warmA. One library (D5236_Trc_warmA) is from a later sequencing batch at 126 bp.
• All runs come from NCBI .sra archives checked against NCBI’s MD5s, with read counts checked against the manifest on conversion.
• The A and B libraries of each cell have nearly identical expression profiles and cannot be distinguished genetically from libraries of other treatments, so they may be subsamples of one culture; if so, the error model understates variability and significance is optimistic. The record carries the flag replicate_culture_independence_unverified.

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

Harmonized evidence. Processed input. Input SHA-256: 2bae06ceaff293aaaa0e3dbf9ec6cce42ea0b18c4028ba6ef4e2a374cfeee32b.

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_OA_RNASEQ_PRJNA826964

Phenotype interpretation: The BioProject title frames acidification as compromising energy management; AREE records the hepatopancreas transcriptional response to acidification, not a measured organism-level energetic or survival phenotype

Biological replication: 6 pooled RNA samples, one per arm at each of 7, 28 and 56 days, each sequenced as three libraries (18 libraries); the BioSample records call the libraries biological replicates, but their genotypes show each set of three is one pool of several oysters

Evidence classification: stress_response. Tissue: hepatopancreas; life stage: not_recorded.

Quality flags: raw_reanalysis;ocean_acidification_response;timepoint_blocked_contrast;pooled_rna_samples;possible_genetic_background_confound.

Study limitations:

• No publication is linked to the BioProject, and searches of PubMed, Europe PMC full text and Crossref on 2026-09-28 found none, so there are no published methods, results or effect tables to reconcile the reanalysis against.
• The acidification intensity (target pH or pCO2), seawater carbonate chemistry, temperature and oyster size or age are not recorded in the public metadata, so exposure intensity and life stage are unresolved.
• The treatment was probably CO2-driven acidification to pH 7.50. This is inferred, not documented: the same IOCAS group (L. Qiu and colleagues) ran C. gigas CO2 exposures at pH 7.50 sampled from 7 to 56 days (Wang et al. 2021, Ecotoxicol Environ Saf, doi:10.1016/j.ecoenv.2021.112235) and at pH 7.50 for 7 and 60 days (Wang et al. 2020, Sci Total Environ, doi:10.1016/j.scitotenv.2020.140177), and reported hepatopancreas responses to acidification over about two months (Zhang et al. 2021, J Oceanol Limnol, doi:10.1007/s00343-021-0462-x). None of these papers is linked to PRJNA826964, and the closed-access hepatopancreas paper, the most likely companion, has not been checked against it.
• The primary AREE contrast compares the three acidified pools with the three control pools and blocks on sampling day (~ timepoint + condition); it estimates an acidification effect averaged over 7, 28 and 56 days rather than time-specific or acclimation effects, and it has only two residual degrees of freedom.
• The three libraries per day-by-condition cell are technical replicates of one pooled RNA sample, not the independent biological replicates the BioSample attributes state. Expressed-SNP allele frequencies (scripts/check_replicate_genotypes.py, 4M read pairs per library) agree within a cell to within resequencing noise and show no single-animal genotype peaks, and within-cell expression dispersion is 2.7% BCV against 10.8-22.4% in the other AREE oyster studies. Treating the 18 libraries as replicates inflates significance roughly twelvefold, so the libraries are summed into 6 pools (–collapse-by=condition+timepoint).
• Each pool is a different set of animals, and the acidified pools are genetically further from the controls (mean allele-frequency difference 0.24-0.31) than the control pools are from one another (0.085-0.19), so acidified and control oysters may come from different stocks or families. Several of the strongest effects are 4-6 log2 changes in transposon-derived genes (tigger, HARBI1), the pattern expected from presence-absence variation between genetic backgrounds, so part of the contrast may be genetic rather than an acidification response. The evidence is harmonized with every row flagged pooled_rna_samples and possible_genetic_background_confound, so scoring discounts it and evidence cards list the caveat; treat it as provisional acidification evidence until a design with shared genetic backgrounds confirms it.
• Condition, sampling day and replicate were taken from NCBI BioSample treatment and replicate attributes and agree with the library names (C/O = control/acidified, followed by day and replicate).
• The BioProject carries no author-deposited processed expression matrix.

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

Harmonized evidence. Processed input. Input SHA-256: 4a01845d837665c4e977190e7e9111a2d5a7bd3e5f38d89ca473276a96b26f2c.

CGIG_OSHV1_RNASEQ_PRJNA1329250

Phenotype interpretation: Infection up-regulated antiviral defense transcripts, including RIG-I-like receptors and the interferon-like pathway, similarly in both lineages; AREE records molecular antiviral responsiveness, not an organism-level survival difference

Biological replication: 42 RNA-seq libraries: 12 controls (6 Midori, 6 Miyagi) and 30 OsHV-1 microvariant-challenged (15 Midori, 15 Miyagi, split across USA, Australia, and France viral strains at 5 libraries per lineage-strain cell)

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

Quality flags: raw_reanalysis;pathogen_challenge_response;lineage_balanced_contrast.

Study limitations:

• This intake represents the molecular antiviral response to experimental OsHV-1 microvariant challenge, not a measured survival or organism-level disease-resistance difference between the two lineages.
• Challenge dose, exposure duration, and time of sampling after inoculation are not recorded in the public SRA metadata, so exposure intensity and duration are unresolved.
• The challenged and control arms are unequal in size (30 versus 12 libraries), but lineage is balanced within each arm and within every viral strain: 6 Midori and 6 Miyagi controls, and 5 of each lineage for each of the Australia, France, and USA strains. The lineage effect is therefore not confounded with infection status, and AREE blocks on lineage as ~ population + condition.
• The publication contrasts the USA and Australia microvariant strains and reports no marked difference between them; the France-strain libraries are present in the BioProject and are pooled into the challenged arm of the AREE contrast rather than analyzed as a separate strain effect.
• The BioProject carries no author-deposited processed expression matrix, so AREE has no published feature-level effect table to reconcile against.
• Condition, lineage, and viral-strain assignments were reconstructed from NCBI BioSample attribute tags rather than from a supplementary sample table; the source metadata spells the Miyagi lineage ‘Myagi’, which AREE normalized.

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

Harmonized evidence. Processed input. Input SHA-256: 3beb15844b8040ff58c64acd452381f853bbbacb730cce2bf434b6ee05d41f2e.

CGIG_PESTO_F0_RNASEQ_PRJEB58194

Phenotype interpretation: The publication found no difference in embryo-larval abnormalities at 24 hpf, disturbed swimming, larger and heavier exposed larvae at some times, a lower epinephrine-induced metamorphosis rate and higher field survival, and differential expression of developmental genes (Hox orthologues, cell-cycle regulators) in gastrulae. AREE records the transcriptional response averaged over two stages.

Biological replication: 36 libraries: 18 control and 18 exposed, nine per stage (gastrula, D larva), labelled with group digits 1-3 and replicate letters A-F.

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

Quality flags: raw_reanalysis;pollutant_exposure_response;pesticide_mixture;pooled_libraries;stage_blocked_contrast;direct_exposure;fdr_lt_0.05.

Study limitations:

• One control D-larva sample title (BT2Ed) is attached to two runs (ERR10659105, ERR10659106); both are kept with the run accession appended to the replicate, and the expressed-SNP check tests whether they are one sample.
• The exposure is a mixture of 18 pesticides and metals at environmentally relevant concentration (nominal sum 2.85 ug/L; measured 3.74 ug/L in F0) during embryo-larval development (0-48 h post fertilization) at the Ifremer Bouin hatchery.
• Each library is presumably a pool of many embryos or larvae; pool size, culture vessels and the meaning of the F0 group digits (1-3) are not recorded in the public metadata, and pools were checked with the expressed-SNP test (scripts/check_replicate_genotypes.py) before analysis.
• All runs come from NCBI .sra archives checked against NCBI’s MD5s (11 F0 runs have no ENA FASTQ), with read counts checked against the NCBI spot counts on conversion.
• The study also deposited F0 pediveligers (sampled after exposure) and F1 offspring exposed in both generations (EE); AREE does not use them.

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

Harmonized evidence. Processed input. Input SHA-256: 5eb3fa1130b516be240eecebcd8c88a5b405a6739f99d273764f3054814af5bb.

CGIG_PESTO_F1DIRECT_RNASEQ_PRJEB58194

Phenotype interpretation: The publication found that the parents’ exposure shaped the offspring phenotype more than direct exposure did; offspring of exposed parents had lower epinephrine-induced metamorphosis and field survival. AREE records the transcriptional response to direct exposure averaged over two stages.

Biological replication: 12 libraries: 6 TT and 6 TE, three per stage.

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

Quality flags: raw_reanalysis;pollutant_exposure_response;pesticide_mixture;pooled_libraries;stage_blocked_contrast;shared_control_group;dependence_group=PRJEB58194_F1_TT;direct_exposure.

Study limitations:

• The two F1 records (direct exposure TE and parental exposure ET) test against the same six TT libraries, so they carry the dependence group PRJEB58194_F1_TT; only the direct-exposure record is harmonized.
• The exposure is a mixture of 18 pesticides and metals at environmentally relevant concentration (nominal sum 2.85 ug/L; measured 3.74 ug/L in F0) during embryo-larval development (0-48 h post fertilization) at the Ifremer Bouin hatchery.
• Each library is presumably a pool of many embryos or larvae; pool size, culture vessels and the meaning of the F0 group digits (1-3) are not recorded in the public metadata, and pools were checked with the expressed-SNP test (scripts/check_replicate_genotypes.py) before analysis.
• All runs come from NCBI .sra archives checked against NCBI’s MD5s (11 F0 runs have no ENA FASTQ), with read counts checked against the NCBI spot counts on conversion.
• The study also deposited F0 pediveligers (sampled after exposure) and F1 offspring exposed in both generations (EE); AREE does not use them.

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

Harmonized evidence. Processed input. Input SHA-256: eeb95c68cdb8cacd7c256a0616f24042aaa54da88a33682cf82f476119e25b62.

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;fdr_lt_0.05;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.

CGIG_VCRASSOSTREAE_RNASEQ_PRJNA515169

Phenotype interpretation: Virulent V. crassostreae J2-9 killed about 60% of oysters within 3 days, through contact-dependent hemocyte lysis requiring the r5.7 gene. AREE records the 8 h whole-spat transcriptional response to infection, not survival per library.

Biological replication: 6 libraries, each a pool of 30 spat: one mock and one V. crassostreae J2-9 pool from each of three independent infection experiments. Pools of 30 animals average out individual variation, so replication is at the level of experiments.

Evidence classification: disease_associated. Tissue: whole_organism; life stage: spat.

Quality flags: raw_reanalysis;pathogen_challenge_response;pooled_libraries;experiment_blocked_contrast;shared_control_group;dependence_group=PRJNA515169_mock_pools;virulent_vibrio_crassostreae;deseq2_significance_unavailable.

Study limitations:

• The two AREE records from this study (the other is CGIG_VTASMANIENSIS_RNASEQ_PRJNA515169, V. tasmaniensis LGP32) test against the same three mock-injected pools, so they carry the dependence group PRJNA515169_mock_pools and count as one replication group.
• Replicate numbers in the sample aliases are taken to identify the independent infection experiment, as the publication describes one pool per condition per experiment; the model blocks on experiment (~ experiment + condition).
• The mock control is an injection of sterile seawater, so the contrast isolates the response to the bacteria, not to injection; the study’s untreated oysters and its nonvirulent strains (V. tasmaniensis LMG20012T, V. crassostreae J2-8) are not used.
• The publication reports 331 oyster genes modulated by Vibrio relative to mock across strains, analysed in the IHPE Galaxy pipeline; AREE quantifies against GCF_963853765.1/RS_2024_06 with Salmon and DESeq2.
• ENA served the FASTQs at 0.05-0.35 MB/s in October 2026, so the five runs that had not arrived intact (SRR8551080, SRR8551081, SRR8551083, SRR8551087, SRR8551091: one mock, one J2-9 and all three LGP32 pools) were taken from NCBI .sra archives instead (CGIG_VIBRIO_RNASEQ_PRJNA515169_sra_locations.tsv). Each library comes from a single source.

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

Harmonized evidence. Processed input. Input SHA-256: c3f3c2871db357f202ace0a460515cf823255d294a67864d4284126428ed56d0.

CGIG_VTASMANIENSIS_RNASEQ_PRJNA515169

Phenotype interpretation: Virulent V. tasmaniensis LGP32 killed about 60% of oysters within 3 days, through phagocytosis-dependent hemocyte lysis requiring intracellular T6SS effectors. AREE records the 8 h whole-spat transcriptional response to infection, not survival per library.

Biological replication: 6 libraries, each a pool of 30 spat: one mock and one V. tasmaniensis LGP32 pool from each of three independent infection experiments. Pools of 30 animals average out individual variation, so replication is at the level of experiments.

Evidence classification: disease_associated. Tissue: whole_organism; life stage: spat.

Quality flags: raw_reanalysis;pathogen_challenge_response;pooled_libraries;experiment_blocked_contrast;shared_control_group;dependence_group=PRJNA515169_mock_pools;virulent_vibrio_tasmaniensis;deseq2_significance_unavailable.

Study limitations:

• The two AREE records from this study (the other is CGIG_VCRASSOSTREAE_RNASEQ_PRJNA515169, V. crassostreae J2-9) test against the same three mock-injected pools, so they carry the dependence group PRJNA515169_mock_pools and count as one replication group.
• Replicate numbers in the sample aliases are taken to identify the independent infection experiment, as the publication describes one pool per condition per experiment; the model blocks on experiment (~ experiment + condition).
• The mock control is an injection of sterile seawater, so the contrast isolates the response to the bacteria, not to injection; the study’s untreated oysters and its nonvirulent strains (V. tasmaniensis LMG20012T, V. crassostreae J2-8) are not used.
• The publication reports 331 oyster genes modulated by Vibrio relative to mock across strains, analysed in the IHPE Galaxy pipeline; AREE quantifies against GCF_963853765.1/RS_2024_06 with Salmon and DESeq2.
• ENA served the FASTQs at 0.05-0.35 MB/s in October 2026, so the five runs that had not arrived intact (SRR8551080, SRR8551081, SRR8551083, SRR8551087, SRR8551091: one mock, one J2-9 and all three LGP32 pools) were taken from NCBI .sra archives instead (CGIG_VIBRIO_RNASEQ_PRJNA515169_sra_locations.tsv). Each library comes from a single source.

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

Harmonized evidence. Processed input. Input SHA-256: 5d73a1e8fde80d460f9fd8139da0c2ff4bf0c58c1a2f0d5e1d0afadc8147c53d.

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.