Evidence card: NCBI:GeneID:117684421

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
CGIG_HEAT24H_RNASEQ_PRJNA407831	protein starmaker	35C_24h_vs_0h_gill	log2 fold change	-0.5508	0.45	not available	Study-level association; see design caveats
CGIG_HEAT6H_RNASEQ_PRJNA407831	protein starmaker	35C_6h_vs_0h_gill	log2 fold change	0.2777	0.5891	0.8896	Study-level association; see design caveats
PRJEB86646	protein starmaker	30C_vs_23C_fed_before_oshv1	log2 fold change	-0.8018	0.1635	8.836e-06	Study-level association; see design caveats
PRJNA593309	protein starmaker	29C_vs_21C_12h_oshv1_cohabitation	log2 fold change	0.3873	0.6213	0.9215	Study-level association; see design caveats
PRJNA735889	protein starmaker	ph_6.5_6.8_vs_ph_7.4_7.8_23d_juveniles	log2 fold change	-0.2602	0.1994	0.4151 (nominal only)	Exploratory; tank clustering unmodeled
PRJNA1329250	protein starmaker	oshv1_microvariant_challenge_vs_unchallenged_control	log2 fold change	-0.1323	0.2136	0.7218	Study-level association; see design caveats
PRJEB58194	protein starmaker	pesticide_mixture_TE_vs_TT_F1_gastrula_pediveliger	log2 fold change	-1.61	0.3196	0.001925	Study-level association; see design caveats
PRJEB86618	protein starmaker	starved_vs_fed_ad_libitum_16d_before_oshv1	log2 fold change	-0.1158	0.3411	0.8087	Study-level association; see design caveats
CGIG_VCRASSOSTREAE_RNASEQ_PRJNA515169	protein starmaker	vibrio_crassostreae_J2_9_vs_mock_injection_8h	log2 fold change	-0.8469	0.3181	0.185	Study-level association; see design caveats
CGIG_VTASMANIENSIS_RNASEQ_PRJNA515169	protein starmaker	vibrio_tasmaniensis_LGP32_vs_mock_injection_8h	log2 fold change	-0.8174	0.2864	0.1055	Study-level association; see design caveats

CGIG_HEAT24H_RNASEQ_PRJNA407831

Phenotype interpretation: Intertidal-origin F1 oysters showed higher survival after acute heat stress (42 C, 1 h) and higher metabolic rates at 35 C than subtidal-origin oysters, with slower growth, and more transcriptional plasticity. AREE records the gill transcriptional response to 35 C averaged over the four populations, not survival per library.

Biological replication: 23 libraries analysed (24 sequenced; one 0 h outlier left out): 11 at 0 h and 12 at 24 h. Each library pools equal gill RNA from five oysters of one culture tank; four populations (two sites x intertidal or subtidal origin) x three tanks, and the same tanks are sampled at each time.

Evidence classification: stress_response. Tissue: gill; life stage: adult.

Quality flags: raw_reanalysis;acute_heat_response;pooled_libraries;population_blocked_contrast;shared_control_group;dependence_group=PRJNA407831_0h_pools;heat_24h;deseq2_significance_unavailable.

Study limitations:

Both AREE records from this study (the other is CGIG_HEAT6H_RNASEQ_PRJNA407831, 6 h) test against the same twelve 0 h pools, so they carry the dependence group PRJNA407831_0h_pools and count as one replication group.
Each library pools gill RNA of five oysters, so the error model describes tank-pool variation, not variation between animals. The sister IOCAS study PRJNA826964 deposited resequenced RNA as replicates, so these pools were checked with the expressed-SNP test (scripts/check_replicate_genotypes.py) before analysis.
The model blocks on the four source populations (~ population + condition), so the effect is averaged over intertidal and subtidal origins and the two sites; the publication’s main result, that intertidal oysters respond with more plasticity, is not part of this record. A tank-paired model (~ tank + condition) is kept as a sensitivity analysis.
Sample aliases code tidal origin as J or X (for example BYQJ01, LTX243); the publication uses I (intertidal) and S (subtidal), and the BioSamples do not record it. J and X are read as the Chinese jian (intertidal) and xia (subtidal), but no AREE result depends on that reading because population is a blocking factor.
One 0 h library, h0_LTJ_2, is left out by AREE’s QC rule (median VST correlation below the median minus three robust SDs); it is the library the publication also discarded (LT-I_0h_2). The exclusion lives in scripts/prepare_prjna407831_fastqs.py.
ENA served other studies at 0.05-0.35 MB/s in October 2026, so all runs come from NCBI .sra archives checked against NCBI’s MD5s, with read counts checked against the manifest on conversion.

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

Harmonized evidence. Processed input. Input SHA-256: ba65a504fd1c43fe5df5636afd198fc3f2b95abd6a145604c6ed9ca3caf03421.

CGIG_HEAT6H_RNASEQ_PRJNA407831

Biological replication: 23 libraries analysed (24 sequenced; one 0 h outlier left out): 11 at 0 h and 12 at 6 h. Each library pools equal gill RNA from five oysters of one culture tank; four populations (two sites x intertidal or subtidal origin) x three tanks, and the same tanks are sampled at each time.

Evidence classification: stress_response. Tissue: gill; life stage: adult.

Quality flags: raw_reanalysis;acute_heat_response;pooled_libraries;population_blocked_contrast;shared_control_group;dependence_group=PRJNA407831_0h_pools;heat_6h.

Study limitations:

Both AREE records from this study (the other is CGIG_HEAT24H_RNASEQ_PRJNA407831, 24 h) test against the same twelve 0 h pools, so they carry the dependence group PRJNA407831_0h_pools and count as one replication group.
Each library pools gill RNA of five oysters, so the error model describes tank-pool variation, not variation between animals. The sister IOCAS study PRJNA826964 deposited resequenced RNA as replicates, so these pools were checked with the expressed-SNP test (scripts/check_replicate_genotypes.py) before analysis.
The model blocks on the four source populations (~ population + condition), so the effect is averaged over intertidal and subtidal origins and the two sites; the publication’s main result, that intertidal oysters respond with more plasticity, is not part of this record. A tank-paired model (~ tank + condition) is kept as a sensitivity analysis.
Sample aliases code tidal origin as J or X (for example BYQJ01, LTX243); the publication uses I (intertidal) and S (subtidal), and the BioSamples do not record it. J and X are read as the Chinese jian (intertidal) and xia (subtidal), but no AREE result depends on that reading because population is a blocking factor.
One 0 h library, h0_LTJ_2, is left out by AREE’s QC rule (median VST correlation below the median minus three robust SDs); it is the library the publication also discarded (LT-I_0h_2). The exclusion lives in scripts/prepare_prjna407831_fastqs.py.
ENA served other studies at 0.05-0.35 MB/s in October 2026, so all runs come from NCBI .sra archives checked against NCBI’s MD5s, with read counts checked against the manifest on conversion.

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

Harmonized evidence. Processed input. Input SHA-256: 3ff5b26926b5dc5ac2b94196d5b5a8628742dc7a4ebf2460da80389567311c2a.

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;fdr_lt_0.05;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_HEAT_RNASEQ_PRJNA593309

Phenotype interpretation: Survival 14 days after cohabitation was higher at 29 C (85.7%) than at 21 C (52.4%), and viral load rose more slowly at 29 C. AREE records the whole-oyster transcriptional difference at 12 h, not survival per library.

Biological replication: 5 oysters from 6 libraries: three at 21 C, each from a different tank, and two at 29 C, because two of the three 29 C libraries are the same oyster and were summed. The publication describes one oyster per tank, so the duplicated 29 C oyster means either one tank was sampled twice or one RNA was sequenced twice.

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

Quality flags: raw_reanalysis;temperature_response;during_oshv1_infection;duplicate_animal_libraries_collapsed;one_oyster_per_tank;dependence_group=PRJNA593309_21C_tanks.

Study limitations:

Both arms are infected, so the contrast is temperature in the context of early OsHV-1 infection, not temperature alone; before infection the publication finds only nine genes differing between 29 and 21 C.
One whole oyster per tank was sequenced at each time point, with three replicate tanks per temperature (45 l tanks), so libraries are tank-level replicates and the contrast has three tanks per arm.
The two AREE records from this study use different oysters but the same three 21 C tanks (the 21 C 12 h oysters of CGIG_HEAT_RNASEQ_PRJNA593309 and the 21 C 0 h and 48 h oysters of CGIG_OSHV1_RNASEQ_PRJNA593309), so both carry the dependence group PRJNA593309_21C_tanks and count as one replication group.
The BioSamples give a collection date of 2019-05-19, but the publication dates the experiment to May 2016; the experimental groups follow the sample aliases (Cg_<CTR | OsHV>hpc_), which agree with the publication’s design.
The study also deposited libraries at 26 C and at 24 and 96 h; the publication does not analyse the 26 C libraries, and AREE uses only the time points of its two contrasts.
The publication aligned reads with STAR to the Ensembl oyster genome v9.38 and tested with edgeR; AREE quantifies against GCF_963853765.1/RS_2024_06 with Salmon and DESeq2.
Two of the three 29 C libraries at 12 h are the same oyster by expressed-SNP genotype, so this record has two independent 29 C oysters, little power, and fewer significant genes than the publication, whose three-replicate analysis counted that oyster twice.
Mapping is about eight points lower at 29 C than at 21 C at 12 h, a systematic shift that may reflect more viral or unspliced RNA at 29 C or a batch difference.

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

Harmonized evidence. Processed input. Input SHA-256: 539c129666a98b1b71f771636b53a7cd9cbc55ce3de8bb6fe3f1a9a51bfa4c30.

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;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_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_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;fdr_lt_0.05.

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;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.

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.

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.