Biology subjects

Walkowiak, B.

Publications and source records attributed to Walkowiak, B..

3 recordsLinked to original sources

bioRxiv2026

Engineering chromatin to encode transcriptional immune memory in Arabidopsis

Transcriptional memory enables organisms to respond more rapidly to recurrent stress, yet the underlying features of chromatin that contribute to this transcriptional recalibration remain poorly defined. Here we identify the genes displaying transcriptional memory in response to the bacterial immune elicitor, flg22, in Arabidopsis thaliana. In comparison to non-memory response genes, these memory genes show a preference for tissue-specific over uniform spatial expression patterning. The chromatin architecture of these genes in the resting state displays depletion of H3K4me3, elevation H3K27me3 and a subset are marked by H3K27me3-H3K4me3 bivalency. The H3K4me3 demethylase, JMJ14, is required for transcriptional memory, with JMJ14 occupancy enriched over memory gene loci. Upon priming, chromatin is reconfigured, with H3K4me3 levels increasing in a sustained manner at memory gene loci. To assess the function of this H3K4me3 accrual, we employ epigenome-engineering, observing that its targeted deposition at memory gene loci, including the WRKY29 locus, is sufficient to drive transcriptional memory and can endow plants with enhanced resistance to the bacterial pathogen, Pseudomonas syringae. Together, the findings demonstrate a causal role for H3K4me3 in transcriptional memory, under the regulation of JMJ14, and open the door for rational rewriting of chromatin to enhance organismal resilience.

plant biology↗

bioRxiv2026

Embryonic origin of cancer in newborn twins

Studying monozygotic twins who present with identical cancers informs on the developmental origins of childhood tumours. Here, we performed whole genome sequencing on multiple tumour, normal, and placental samples to reconstruct the phylogeny of a soft tissue cancer that spread in utero between monozygotic twins. This generalisable and scalable approach allows us to dissect the earliest stages of twinning, revealing unexpected asymmetrical contributions of embryonic lineages to the placenta and each twin.

cancer biology↗

bioRxiv2024

No evidence of immunosurveillance in mutation-hotspot driven clonal haematopoiesis

The theory of immunosurveillance posits that T-cells can selectively eliminate clones harbouring non-self antigens generated by somatic mutations. There is considerable evidence supporting the role of immune surveillance in cancer. Whether immunosurveillance imposes a negative selective pressure on pre-cancerous clones, however, is not well established. Here, we studied the association between MHC-variant binding and risk of clonal haematopoiesis (CH), a pre-cancer state in the blood driven by expansions of mutant haematopoietic stem cells (HSCs). We predicted MHC binding affinity towards 40 known CH hotspot variants in 380,000 UK Biobank participants, and examined the relationship between predicted binding to each variant and risk of its expansion in the blood. Despite being well powered to detect subtle differences in selective pressure, we did not find associations between predicted MHC binding and CH prevalence for any of the hotspot variants. In individuals in whom we identified CH, there was no relationship between predicted binding affinity to the variant and size of the clone. Overall, we do not find evidence for the MHC genotype to be a factor that affects which somatic variants expand in CH, suggesting a limited role for immunosurveillance in shaping the genetic diversity of the blood.

genomics↗