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  • 1
    In: Journal of Fish Biology, Wiley, Vol. 101, No. 5 ( 2022-11), p. 1160-1181
    Abstract: Groups of basking sharks engaged in circling behaviour are rarely observed, and their function remains enigmatic in the absence of detailed observations. Here, underwater and aerial video recordings of multiple circling groups of basking sharks during late summer (August and September 2016–2021) in the eastern North Atlantic Ocean showed groups numbering between 6 and 23 non‐feeding individuals of both sexes. Sharks swam slowly in a rotating “torus” (diameter range: 17–39 m), with individuals layered vertically from the surface to a maximum depth of 16 m. Within a torus, sharks engaged in close‐following, echelon, close‐flank approach or parallel‐swimming behaviours. Measured shark total body lengths were 5.4–9.5 m (mean L T : 7.3 m ± 0.9  s.d. ; median: 7.2 m, n  = 27), overlapping known lengths of sexually mature males and females. Males possessed large claspers with abrasions that were also observed on female pectoral fins. Female body colouration was paler than that of males, similar to colour changes observed during courtship and mating in other shark species. Individuals associated with most other members rapidly (within minutes), indicating toroidal behaviours facilitate multiple interactions. Sharks interacted through fin–fin and fin–body contacts, rolling to expose the ventral surfaces to following sharks, and breaching behaviour. Toruses formed in late summer when feeding aggregations in zooplankton‐rich thermal fronts switched to non‐feeding following and circling behaviours. Collectively, the observations explain a courtship function for toruses. This study highlights northeast Atlantic coastal waters as a critical habitat supporting courtship reproductive behaviour of endangered basking sharks, the first such habitat identified for this species globally.
    Type of Medium: Online Resource
    ISSN: 0022-1112 , 1095-8649
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 410564-3
    detail.hit.zdb_id: 1471958-7
    SSG: 21,3
    SSG: 12
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  • 2
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 142, No. 4 ( 2020-07-28), p. 324-338
    Abstract: Long QT syndrome (LQTS) is a rare genetic disorder and a major preventable cause of sudden cardiac death in the young. A causal rare genetic variant with large effect size is identified in up to 80% of probands (genotype positive) and cascade family screening shows incomplete penetrance of genetic variants. Furthermore, a proportion of cases meeting diagnostic criteria for LQTS remain genetically elusive despite genetic testing of established genes (genotype negative). These observations raise the possibility that common genetic variants with small effect size contribute to the clinical picture of LQTS. This study aimed to characterize and quantify the contribution of common genetic variation to LQTS disease susceptibility. Methods: We conducted genome-wide association studies followed by transethnic meta-analysis in 1656 unrelated patients with LQTS of European or Japanese ancestry and 9890 controls to identify susceptibility single nucleotide polymorphisms. We estimated the common variant heritability of LQTS and tested the genetic correlation between LQTS susceptibility and other cardiac traits. Furthermore, we tested the aggregate effect of the 68 single nucleotide polymorphisms previously associated with the QT-interval in the general population using a polygenic risk score. Results: Genome-wide association analysis identified 3 loci associated with LQTS at genome-wide statistical significance ( P 〈 5×10 −8 ) near NOS1AP , KCNQ1 , and KLF12 , and 1 missense variant in KCNE1 (p.Asp85Asn) at the suggestive threshold ( P 〈 10 −6 ). Heritability analyses showed that ≈15% of variance in overall LQTS susceptibility was attributable to common genetic variation ( h2SNP 0.148; standard error 0.019). LQTS susceptibility showed a strong genome-wide genetic correlation with the QT-interval in the general population (r g =0.40; P =3.2×10 −3 ). The polygenic risk score comprising common variants previously associated with the QT-interval in the general population was greater in LQTS cases compared with controls ( P 〈 10−13), and it is notable that, among patients with LQTS, this polygenic risk score was greater in patients who were genotype negative compared with those who were genotype positive ( P 〈 0.005). Conclusions: This work establishes an important role for common genetic variation in susceptibility to LQTS. We demonstrate overlap between genetic control of the QT-interval in the general population and genetic factors contributing to LQTS susceptibility. Using polygenic risk score analyses aggregating common genetic variants that modulate the QT-interval in the general population, we provide evidence for a polygenic architecture in genotype negative LQTS.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 1466401-X
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