Husson, C. | Search bioRxiv

bioRxiv2026

Homologous recombination delayed repair in oocytes in the bdelloid rotifer Adineta vaga post radiation

Bdelloid rotifers are known to survive desiccation and high doses of ionizing radiation. This extreme resistance is notably due to their capacity to cope with numerous DNA double-strand breaks (DSBs). Genes encoding key components of the non-homologous end joining (NHEJ) DNA repair pathway are strongly upregulated in the bdelloid rotifer Adineta vaga following exposure to ionizing radiation. Considering the notably high doses tolerated by these organisms, their capacity to efficiently restore genome integrity is particularly striking. Although NHEJ is generally regarded as less accurate than homologous recombination (HR), the absence of major genomic rearrangements in the descendants of irradiated rotifers suggests that DNA repair occurs with high fidelity. Terwagne et al. recently reported a delayed repair in germline nuclei, occurring during oocyte development when homologous chromosomes pair, thereby enabling template-based repair through HR. In this study, we established an in situ hybridization approach on A. vaga cryosections to investigate the spatial and temporal expression of key actors involved in NHEJ, HR, and Base excision repair (BER) pathways in somatic and germline tissues. We show that NHEJ (KU80) and BER-related genes (PARPs) as well as A. vaga Ligase E (putatively involved in DNA repair) are expressed early after radiation exposure in the somatic syncytium. In contrast, HR-related genes (Rad51: two paralogs, Rad54), as well as PCNA (involved in DNA replication, NER, BER, HR) are expressed later in maturing oocytes, indicating the activation of a delayed homologous recombination repair pathway in germline nuclei. Nurse cells, which express genes associated with both HR and NHEJ pathways, may rely on both mechanisms for their own DNA repair while also supplying mRNAs to the maturing oocyte. Our results provide new evidence for a differential regulation of DNA DSB repair pathways between soma and germline in bdelloids, with NHEJ predominating in somatic tissues and HR in the germline of A. vaga. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/722046v1_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@3b1f3borg.highwire.dtl.DTLVardef@17f5eb5org.highwire.dtl.DTLVardef@122ef14org.highwire.dtl.DTLVardef@7e4413_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOAbstract Figure:C_FLOATNO Summary of in situ hybridization results: genes coding for actors of NHEJ are expressed in the somatic nuclei and in the nurse nuclei of Adineta vaga individuals 2.5 hours post X-rays radiation, while genes coding for HR actors and PCNA (involved in multiple pathways including DNA replication and DNA repair: NER, BER, MR, HR) are expressed in the nurse nuclei 2.5 hours post radiation, and later in the maturing oocyte during oogenesis and in the laid eggs. Genes coding for actors highly expressed post-radiation, involved in the BER pathway appear to be only expressed in the somatic syncytium 2.5 hours post radiation, as well as the gene coding for the Ligase E, likely involved in DNA repair. C_FIG

molecular biology↗

bioRxiv2022

Ability of the Ash dieback pathogen to reproduce and to induce damage on its host are controlled by different environmental parameters

Ash dieback, induced by an invasive ascomycete, Hymenoscyphus fraxineus, has emerged in the last decade as a severe disease threatening ash populations in Europe. Future prospects for Ash are improved by the existence of individuals with natural genetic resistance to the disease and by limited disease impact in many environmental conditions where ashes are frequent. Nevertheless, it was suggested that even in those conditions, ash trees are infected and enable pathogen transmission. We studied the influence of climate and local environment on the ability of H. fraxineus to infect, be transmitted and cause damage on its host. We showed that healthy carrier, i.e. asymptomatic individuals carrying H. fraxineus, exists and may play a significant role in ash dieback epidemiology. Environment strongly influenced H. fraxineus with different parameters being important depending on the life cycle stage. The ability of H. fraxineus to establish on ash leaves and to reproduce on the leaf debris in the litter (rachises) mainly depended on total precipitations in July-August and was not influenced by local tree cover. By contrast, damages to the host, and in particular shoot mortality was significantly reduced by high summer temperature in July-August and by high autumn average temperature. As a consequence, in many situations ash trees are infected and enable H. fraxineus transmission while showing limited or even no damages. We also observed a decreasing trend of severity (leaf necrosis and shoot mortality likelihood) with the time of disease presence in a plot that could be significant for the future of Ash dieback.

ecology↗

bioRxiv2017

The ash dieback invasion of Europe was founded by two individuals from a native population with huge adaptive potential

Accelerating international trade and climate change make pathogen spread an increasing concern. Hymenoscyphus fraxineus, the causal agent of ash dieback is one such pathogen, moving across continents and hosts from Asian to European ash. Most European common ash (Fraxinus excelsior) trees are highly susceptible to H. fraxineus although a small minority (~5%) evidently have partial resistance to dieback. We have assembled and annotated a draft of the H. fraxineus genome which approaches chromosome scale. Pathogen genetic diversity across Europe, and in Japan, reveals a tight bottleneck into Europe, though a signal of adaptive diversity remains in key host interaction genes (effectors). We find that the European population was founded by two divergent haploid individuals. Divergence between these haplotypes represents the 'shadow' of a large source population and subsequent introduction would greatly increase adaptive potential and the pathogen's threat. Thus, EU wide biological security measures remain an important part of the strategy to manage this disease.

genomics↗