ALBERT

Description: While originally acquired from the environment, a fraction of the microbiota is transferred from parents to offspring. The immune system shapes the microbial colonization, while commensal microbes may boost host immune defences. Parental transfer of microbes in viviparous animals remains ambiguous, as the two transfer routes (transovarial vs. pregnancy) are intermingled within the maternal body. Pipefishes and seahorses (Syngnathids) are ideally suited to disentangle transovarial microbial transfer from a contribution during pregnancy due to their maternal egg production and their unique male pregnancy. We assessed the persistency and the changes in the microbial communities of the maternal and paternal reproductive tracts over proceeding male pregnancy by sequencing microbial 16S rRNA genes of swabs from maternal gonads and brood pouches of non-pregnant and pregnant fathers. Applying parental immunological activation with heat-killed bacteria, we evaluated the impact of parental immunological status on microbial development. Our data indicate that maternal gonads and paternal brood pouches harbor distinct microbial communities, which could affect embryonal development in a sex-specific manner. Upon activation of the immune system, a shift of the microbial community was observed. The activation of the immune system induced the expansion of microbiota richness during late pregnancy, which corresponds to the time point of larval mouth opening, when initial microbial colonization must take place.

Description: Data table shows life history (size-length) and gene expression measurements of 44 target genes and 4 housekepping genes for 192 samples (F2 juveniles) of the experiment "Grandparental immune priming in Syngnathus typhle". Gene expression was measured using Fluidigm chip systems in May 2014. Shown are the mean Ct values (Cycle time) of two technical replicates.

Description: In this study, we measured the relative transcript expression of 45 target genes and 3 normalizer genes in liver samples of 120 Atlantic salmon that were subjected to 3 different climate scenarios in a tank-based system. Atlantic salmon were exposed to following treatments: (1) Control (CT) constant temperature of 12°C and 100 % air saturation; (2) Warm&Normoxic (WN) incremental temperature increase (1°C per week from 12 - 20°C) at 100% air saturation; and (3) Warm&Hypoxic (WH) decrease in oxygen content of 70% air saturation over one week, followed by two weeks of acclimation to this oxygen level, and then incremental temperature increase (1°C per week from 12 - 20°C) at 70% air saturation. Liver samples were taken from 8 fish per treatment group (CT, WN and WH) at 5 different temperature measuring points: 12°C, 16°C, 18°C, 19°C, and 20°C. For each treatment group, we used 8 biological fish replicates (4 fish from 2 tank replicates). The sampling during the simulated seasonal temperature increase was performed 3 days after reaching the temperature level of interest (12°C-initial, 16°C-3days, 18°C-3days, 19°C-3days, 20°C-3days). Once the maximum temperature increase of 20°C was reached, an additional sampling after 4 weeks at 20°C was carried out (20°C-4weeks). After each temperature challenge eight fish per per tank replicate (n = 8, N = 24) were euthanized with 400 mg L^-1 of tricaine-methane-sulfonate. Liver tissues (100 mg per sample) were rapidly dissected from fish, placed in RNase-free 1.5 mL tubes, flash-frozen in liquid nitrogen, and stored at -80°C until RNA extractions were performed. The relative transcript expression values of 45 genes of interest (GOIs) and 3 normalizers were assessed for 8 individual fish samples per 3 treatment groups at 5 sampling time points (n = 8, N = 120). Real-time qPCR Fluidigm Biomark HD system based on 96.96 dynamic arrays (GE-arrays) was employed according to the manufacturer's instructions (Fluidigm, Biomark HD). The transcript levels of 48 genes were measured in two technical replicates, while we included two no template controls (NTCs), two controls for genomic DNA contamination (no-reverse transcription 'no-RT') and two linker samples for inter-run and between-run calibration. In this data submission file, we provide the 'mean threshold cycle (CT) values' for 45 GOIs and 3 normalizer genes that were calculated from two technical replicates and were measured with GE-fast 96.96 PCR protocol and Fluidigm Biomark HD system. This experiment was performed as part of the project 'Mitigating the Impacts of Climate-Related Challenges on Salmon Aquaculture (MICCSA)' within the years 2017-2020.

Description: The transfer of immunity from parents to offspring (trans-generational immune priming (TGIP)) boosts offspring immune defence and parasite resistance. TGIP is usually a maternal trait. However, if fathers have a physical connection to their offspring, and if offspring are born in the paternal parasitic environment, evolution of paternal TGIP can become adaptive. In Syngnathus typhle, a sex-role reversed pipefish with male pregnancy, both parents invest into offspring immune defence. To connect TGIP with parental investment, we need to know how parents share the task of TGIP, whether TGIP is asymmetrically distributed between the parents, and how the maternal and paternal effects interact in case of biparentalTGIP. We experimentally investigated the strength and differences but also the costs of maternal and paternal contribution, and their interactive biparental influence on offspring immune defence through-out offspring maturation. To disentangle maternal and paternal influences, two different bacteria were used in a fully reciprocal design for parental and offspring exposure. In offspring, we measured gene expression of 29 immune genes, 15 genes associated with epigenetic regulation, immune cell activity and life-history traits. We identified asymmetric maternal and paternal immune priming with a dominating,long-lasting paternal effect. We could not detect an additive adaptive biparental TGIP impact. However, biparental TGIP harbours additive costs as shown in delayed sexual maturity. Epigenetic regulation may play a role both in maternal and paternal TGIP.