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Bandaranayake, C.

Publications and source records attributed to Bandaranayake, C..

2 recordsLinked to original sources

Experimental challenge of Chinook salmon with Tenacibaculum maritimum and Tenacibaculum dicentrarchi fulfils Kochs postulates

The bacterial skin disease tenacibaculosis, caused by Tenacibaculum species, can compromise numerous species of economically important marine fish, including salmonids. While tenacibaculosis is a known threat to Atlantic salmon (Salmo salar) aquaculture, the pathogenesis of Tenacibaculum maritimum and Tenacibaculum dicentrarchi on Chinook salmon (Oncorhynchus tshawytscha) has not yet been investigated. In this study, three molecular O-AGC types of T. maritimum (O-AGC Type 3-0, Type 2-1 and Type 3-2) and T. dicentrarchi isolated during a disease outbreak of farmed Chinook salmon in Aotearoa New Zealand were assessed for their ability to induce tenacibaculosis in salmon smolts under controlled conditions. Naive Chinook salmon were exposed to T. maritimum or T. dicentrarchi by immersion. Clinical signs of tenacibaculosis were apparent post-exposure and observed in 100% of all three molecular O-AGC types of T.-maritimum-challenged fish, with 100% morbidity in O-AGC Type 2-1 and Type 3-2 and 60% in O-AGC Type 3-0. Chinook salmon exposed to T. dicentrarchi showed characteristic clinical signs of disease in 51% of the challenged population, with 28% morbidity. Common gross pathological signs observed for both Tenacibaculum species were congruent with observations on farmed fish in the field, including scale loss, erythematous skin lesion, skin ulcers, fin necrosis, mouth erosion and gill ulceration. Exophthalmia was observed only in T. maritimum-challenged fish, while skin ulcers appeared grossly more severe with exposed musculature in T. dicentrarchi-challenged fish. Pure T. maritimum and T. dicentrarchi cultures were reisolated from the skin and gills of the challenged fish and their identity was confirmed by species-specific PCR and molecular O-AGC typing. Challenge experiments and associated field surveillance (for T. maritimum) did not show the presence of culturable T. maritimum cells in the anterior kidney. This provides compelling evidence that tenacibaculosis in farmed Chinook salmon is an external infectious disease, and that Tenacibaculum is a marine obligate organism that is unable to survive in fish body fluids and does not cause septicaemia. This has repercussions for approaches to experimental challenges with Tenacibaculum species, which must occur by immersion rather than intraperitoneal or intramuscular inoculation, to replicate the natural transmission pathway and to ensure a successful challenge model. This study fulfilled modernised Kochs postulates for the three molecular O-AGC types of T. maritimum and single strain of T. dicentrarchi as aetiological agents of tenacibaculosis in Chinook salmon that cause mortalities with considerable external abnormalities. Author summaryChinook salmon, Oncorhynchus tshawytscha, is the most significant species of Pacific salmon for its large size and nutritional content which makes it a premium choice for aquaculture. In Aotearoa|New Zealand, Chinook salmon is the only marine salmon species farmed. For a decade, the industry was impacted by an undiagnosed skin disease resulting in high mortalities. Disease susceptibility in Chinook salmon is scarcely studied and added to the challenge for a timely diagnosis. This novel research provides insight on disease susceptibility of Chinook salmon and confirms Tenacibaculum species identified in New Zealand pose a high threat to the aquaculture industry. This research has global implications and contributes valuable insights and approaches to disease management that can be applied in British Columbia and Canada where Chinook salmon populations are in decline.

microbiology↗

SUMO protease FUG1, histone reader AL3 and the PRC1 Complex are integral to repeat-expansion induced epigenetic silencing in Arabidopsis thaliana

Epigenetic gene silencing induced by expanded repeats can cause diverse phenotypes ranging from severe growth defects in plants to genetic diseases such as Friedreichs ataxia in humans1. The molecular mechanisms underlying repeat expansion-induced epigenetic silencing remain largely unknown2,3. Using a plant model, we have previously shown that expanded repeats can induce smallRNAs which in turn can lead to epigenetic silencing through the RNA-dependent DNA methylation pathway4,5. Here, using a genetic suppressor screen, we confirm a key role for the RdDM pathway and identify novel components required for epigenetic silencing caused by expanded repeats. We show that FOURTH ULP LIKE GENE CLASS 1 (FUG1) - a SUMO protease, ALFIN-LIKE 3 - a histone reader and LIKE HETEROCHROMATIN 1 (LHP1) - a component of the PRC1 complex are required for repeat expansion-induced epigenetic silencing. Loss of any of these components suppress repeat expansion-associated phenotypes. SUMO protease FUG1 physically interacts with AL3 and perturbing its potential SUMOylation site disrupts its nuclear localisation. AL3 physically interacts with LHP1 of the PRC1 complex and the FUG1-AL3-LHP1 module is essential to confer repeat expansion-associated epigenetic silencing. Our findings highlight the importance post-translational modifiers and histone readers in epigenetic silencing caused by repeat expansions.

genetics↗