Biology subjects

Moghadam, H. K.

Publications and source records attributed to Moghadam, H. K..

3 recordsLinked to original sources

bioRxiv2021

Identification of a new Infectious Pancreatic Necrosis Virus (IPNV) isolate in Atlantic salmon (Salmo salar L.) that causes mortality in resistant fish

Infectious pancreatic necrosis (IPN) is an important viral disease of salmonids that can affect fish during various life cycles. In Atlantic salmon, selecting for genetically resistant animals against IPN has been one of the most highly praised success stories in the history of fish breeding. The findings that resistance against this disease has a significant genetic component, which is mainly controlled by variations in a single gene, has helped to reduce the IPN outbreaks over the past decade to a great extent. In this paper, we present the identification of a new isolate of the IPN virus, from a field outbreak, that had caused mortality, even in the genetically resistant animals. We recovered and assembled the full-length genome of this virus, following deep-sequencing of an infected tissue. The comparative sequence analysis revealed that for the critical amino acid motifs, previously found to be associated with the degree of virulence, the newly identified isolate is similar to the viruss avirulent form. However, we detected a set of deduced amino acid residues, particularly in the hypervariable region of the polyprotein, that collectively are unique to this strain compared to all other reference sequences assessed in this study. We suggest that these mutations have likely equipped the virus with the capacity to escape the host defence mechanism more efficiently, even in the genetically deemed IPN resistant animals.

genomics↗

bioRxiv2020

Polymorphic SINEC_Cf Retrotransposons in the Genome of the Dog (Canis familiaris)

The dog is an exciting genetic system in which many simple and complex traits have now been mapped. For many traits the causal mutation is a polymorphic SINE. To investigate the genome-wide pattern of young SINEC_Cf insertions, we sampled 62 dogs representing 59 breeds and sequenced libraries enriched for SINE flanks. In each dog we detect an average of 10,423 polymorphic loci and all together the libraries identify 81,747 putative polymorphic SINEs. We validated 184 SINEs inserted in protein-coding exons, untranslated regions, introns and intergenic sequence. In dogs both SINEC_Cf and LINEs exhibit a strand bias in introns where antisense copies are more frequent. Antisense polymorphic SINEs also have a higher density in introns. Both SINEs and LINEs drop to very low density near exons. Both sense and antisense polymorphic SINEs also drop to low density upstream of coding exons but not downstream. Antisense polymorphic SINEC_Cfs upstream of coding exons are known to cause narcolepsy, merle, and progressive retinal atrophy in dogs. In other mammals SINE pairs in inverted orientation disrupt gene expression. We find inverted pairs of SINEC_Cf are rare in both introns and intergenic sequence when the two SINEs are separated by less than 100 bp. The lack of inverted pairs is even more pronounced when the SINEs have high sequence identity. Intronic and intergenic LINE pairs show similar patterns. Polymorphic SINEs rarely pair with either SINEC_Cf or SINEC_Cf2. Overall, the high insertion rate of SINEC_Cf provides a natural mutagenesis screen in the dog genome.

genomics↗

bioRxiv2018

Genome-wide association study of piscine myocarditis virus (PMCV) robustness in Atlantic salmon (Salmo salar)

Cardiomyopathy syndrome is a sever, viral disease of Atlantic salmon that mostly affects farmed animals during their late production stage at sea. Caused by piscine myocarditis virus (PMCV), over the past few years, the outbreaks due to this disease have resulted in significant losses to the aquaculture industry. However, there are currently no vaccine that has proven effective against this virus. In this study, using a challenge model, we investigate the genetic variation for robustness to PMCV, by screening large number of animals using a 55 K SNP array. In particular, we aimed to identify genetic markers that are tightly linked to higher disease resistance and can potentially be used in breeding programs. Using genomic information, we estimated heritability of 0.41 {+/-}0.05, suggesting that robustness against this virus is largely controlled by genetic factors. Through association analysis, we identified a major QTL on chromosome 27, explaining approximately 57% of the total additive genetic variation. The region harbouring this putative QTL contains various immune related candidate genes, many of which have previously been shown to have a differential expression profile between the naive and infected animals. We also identified a suggestive association on chromosome 12, where the QTL linked markers are located within two putatively immune related genes. These findings are important as they can be readily implemented into the breeding programs but also the results can further help in fine-mapping the causative mutation, in better understanding the biology of the disease and refine the mechanics of resistance against PMCV.

genomics↗