Biology subjects

Cruickshank, M.

Publications and source records attributed to Cruickshank, M..

2 recordsLinked to original sources

bioRxiv2025

Understanding wood decay diseases in western redcedar through development of ITS-sequencing and qPCR assays

Root and butt rot diseases cause high rates of wood decay in living stands of western redcedar (WRC; Thuja plicata Donn), one of the most valuable forest species in western North America. However, WRC susceptibility and the virulence of wood-decay-causing fungal pathogens are understudied, presenting a high risk for the WRC forest industry. To evaluate susceptibility of WRC to root and butt rot diseases and decay incidence, four pathogenic fungi, including Armillaria ostoyae, Coniferiporia weirii, Heterobasidion occidentale, and Perenniporia subacida, were used to inoculate WRC seedlings using two artificial methods. Next-generation sequencing (NGS) of internal transcribed spacer (ITS) region of the nuclear ribosomal DNA (rDNA) and quantitative polymerase chain reaction (qPCR) assays were developed to evaluate successful infection through detection of targeted pathogens inside the WRC tissues while development of disease was assessed by visual observation of wood decay. Disease incidence rates ranged from 20% to 60% while infection rates ranged from 80% to 100%, validating the effectiveness of the inoculation protocols. The qPCR assays designed with species-specific primers were validated for quantification of absolute abundance of C. weirii inside WRC host tissues with high sensitivity and specificity. These newly developed qPCR assays provide rapid, cost-effective, and accurate tools to detect early infection and latent infection in asymptomatic trees, with wide potential applications for surveillance of C. weirii-caused wood decay disease in greenhouse and field studies, as well as for screening of disease resistance in WRC breeding.

pathology↗

bioRxiv2018

Recapitulation of human germline coding variation in an ultra-mutated infant leukemia

BackgroundMixed lineage leukemia/Histone-lysine N-methyltransferase 2A gene rearrangements occur in 80% of infant acute lymphoblastic leukemia, but the role of cooperating events is unknown. While infant leukemias typically carry few somatic lesions, we identified a case with over 100 somatic point mutations per megabase and here report unique genomic-features of this case.\n\nResultsThe patient presented at 82 days of age, one of the earliest manifestations of cancer hypermutation recorded. The transcriptional profile showed global similarities to canonical cases. Coding lesions were predominantly clonal and almost entirely targeting alleles reported in human genetic variation databases with a notable exception in the mismatch repair gene, MSH2. There were no rare germline alleles or somatic mutations affecting proof-reading polymerase genes POLE or POLD1, however there was a predicted damaging mutation in the error prone replicative polymerase, POLK. The patients diagnostic leukemia transcriptome was depleted of rare and low-frequency germline alleles due to loss-of-heterozygosity, while somatic point mutations targeted low-frequency and common human alleles in proportions that offset this discrepancy. Somatic signatures of ultra-mutations were highly correlated with germline single nucleotide polymorphic sites indicating a common role for 5-methylcytosine deamination, DNA mismatch repair and DNA adducts.\n\nConclusionsThese data suggest similar molecular processes shaping population-scale human genome variation also underlies the rapid evolution of an infant ultra-mutated leukemia.

cancer biology↗