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Kranz, A.

Publications and source records attributed to Kranz, A..

10 recordsLinked to original sources

The chromosome level genome of the Blueberry Stem Gall Wasp, Hemadas nubilipennis (Hymenoptera: Ormyridae) on lowbush blueberry (Vaccinium angustifolium) reveals repeat-driven expansion

Gall-inducing wasps are emerging models for studying plantinsect coevolution, host manipulation, host plant adaptation, and speciation, yet chromosome-level resources remain scarce for most lineages. The blueberry stem gall wasp (BSGW), Hemadas nubilipennis (Hymenoptera: Ormyridae), is native to North America where it induces galls on both lowbush (Vaccinium angustifolium) and highbush blueberries (V. corymbosum). Recently, BSGW has reached outbreak densities in cultivated highbush production. Given that (a) the biology has been characterized primarily from natural lowbush-associated populations, (b) the absence of genomic resources limits comparative analyses, and (c) populations on cultivated highbush represent a recent host shift, we generated the first chromosome-level genome from wild lowbush blueberry. The BSGW genome consists of five chromosome-scale scaffolds totaling 1.08 Gb (N50 = 218 Mb), the second largest known in Chalcidoidea. Comparative analysis reveals that genome size variation is driven primarily by transposable element proliferation (R = 0.96, p < 0.001), with BSGW exhibiting a high proportion of unclassified TEs. Gene-body methylation is conserved, enriched in exons of broadly expressed core genes, and correlates with gene density. The mitochondrial genome (18,697 bp) exhibits extensive gene rearrangement, and COI sequences reveal 4.35.4% divergence from geographically distant populations, suggesting a complex of cryptic species. Additionally, we assemble a near-complete genome of the endosymbiont Wolbachia pipientis (Supergroup A), which encodes PifA and PifB effectors potentially linked to parthenogenesis. These resources establish a foundation for population genomics, taxonomic revision, and applied management, while providing insights into genome architecture, epigenetics, and symbiont interactions.

genomics↗

Elab2ARC: A Browser-Based Workspace for Converting Free-Text Protocols into rich FAIR digital objects

Electronic laboratory notebooks (ELNs) are widely used in the life sciences, but their notebook format limits machine-readability and FAIR compliance. Consequently, researchers often spend significant manual effort restructuring ELN records into publication-ready outputs. We present elab2ARC, a browser-based workspace that automates the conversion of open-source eLabFTW records into Annotated Research Contexts (ARCs)-- version-controlled, ISA-compliant research objects. Using the eLabFTW API, elab2ARC retrieves administrative metadata, protocols, and attachments, reorganising them into ISA-compliant tables and linked datasets. All processing occurs client-side, ensuring user data control before submission to the PLANTdataHUB repository. An optional LLM-assisted workflow extracts structured metadata from free-text protocols, providing editable drafts while preserving human oversight. Designed for use at project completion, elab2ARC reuses existing ELN documentation without disrupting daily laboratory practice. It offers a practical route to FAIR-aligned sharing, publication, and long-term archiving of life-science experimental records. Availability and implementationelab2ARC is freely accessible at https://nfdi4plants.org/elab2arc/. The source code is available at https://github.com/nfdi4plants/elab2arc under a GPL-3.0 license. Supplementary informationSupplementary data are available online.

bioinformatics↗

A haplotype-resolved, chromosome-scale genome assembly for the southern live oak, Quercus virginiana

Hybridization is a major force driving diversification, migration, and adaptation in Quercus species. While population genetics and phylogenetics have traditionally been used for studying these processes, advances in sequencing technology now enable us to incorporate comparative and pan-genomic approaches as well. Here we present a highly contiguous, chromosome-scale and haplotype-resolved genome assembly for the southern live oak, Quercus virginiana, the first reference genome for section Virentes, as part of the American Campus Tree Genomes (ACTG) program. Originating from a clone of Auburn Universitys historic "Toomers Oak," this assembly contributes to the pool of genomic resources for investigating recombination, haplotype variation, and structural genomic changes influencing hybridization potential in this clade and across Quercus. It also provides insights into the architecture of the putative centromeric regions within the genus. Alongside other oak references, the Q. virginiana genome will support research into the evolution and adaptation of the Quercus genus.

genomics↗

A non-catalytic role for MLL2 in controlling chromatin organisation and mobility during the priming of pluripotent cells for differentiation

How the chromatin regulator MLL2 (KMT2B) influences cell differentiation remains poorly understood. MLL2 is the main histone 3 lysine 4 (H3K4) trimethyltransferase acting at bivalent promoters in embryonic stem cells (ESCs) and is required for ESCs to differentiate into neuroectoderm. We show here that this requirement occurs during exit from naive pluripotency, days before neuroectoderm differentiation is impaired. Although MLL2 knockout has only a subtle effect on transcription during exit, reducing the expression of a few important neuroectodermal transcription factors, it substantially remodels chromatin architecture, disrupting 3D chromatin loops associated with bivalent promoters. The enzymatic activity of MLL2 is not needed for stabilising these loops or for neuroectoderm differentiation. This non-catalytic function of MLL2 in stabilising 3D chromatin loops has implications for lineage specification. Because MLL2 shares features with all four MLLs, chromatin tethering, rather than H3K4 methylation, may represent the primary function of MLL proteins during lineage commitment.

cell biology↗

DataPLAN: a web-based data management plan generator for the plant sciences

Research Data Management (RDM) is a system for the effective handling of research data that enables scientists to structure their research questions and ensure best practices throughout the data lifecycle, from acquisition, computation and annotation to data publication and re-use. Data management plans (DMPs) are documents that formally set out the RDM of a project and are required by many funding bodies. DMPs help to organize and structure RDM strategies, thus promoting data findability, accessibility, interoperability and reusability (FAIR). Although DMPs incorporate methods and standards that can be reused by different research projects, the standardization of DMP content is not as evident as the standardization of RDM practices and data/metadata. To address this issue in the plant sciences, we developed DataPLAN - a tool that combines a questionnaire with pre-written standardized responses. We wrapped the questionnaire in a serverless single-page web application that can then generate standardized responses from DMP templates. The current templates cater to plant research grant proposals for Horizon 2020, Horizon Europe and the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG). In the future the range of templates will be extended to accommodate other funding schemes, thereby enabling more users to generate their own templates. The DataPLAN web application is open-source and does not require an internet connection. By utilizing DataPLAN, the workload associated with creating, updating, and adhering to DMPs is significantly reduced.

plant biology↗

Postnatal SETD1B is essential for learning and the regulation of neuronal plasticity genes

Histone 3 lysine 4 methylation (H3K4me) is mediated by six different lysine methyltransferases. Amongst these enzymes SET domain containing 1b (SETD1B) has been linked to syndromic intellectual disability but its role in the postnatal brain has not been studied yet. Here we employ mice that lack Setd1b from excitatory neurons of the postnatal forebrain and combine neuron-specific ChIP-seq and RNA-seq approaches to elucidate its role in neuronal gene expression. We observe that SETD1B controls the expression of genes with a broad H3K4me3 peak at their promoters that represent neuronal enriched genes linked to learning and memory function. Comparative analysis to corresponding data from conditional Kmt2a and Kmt2b knockout mice suggests that this function is specific to SETD1B. Moreover, postnatal loss of Setd1b leads to severe learning impairment, suggesting that SETD1B-mediated regulation of H3K4me levels in postnatal neurons is critical for cognitive function.

neuroscience↗

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte

Histone 3 lysine 4 trimethylation (H3K4me3) is an epigenetic mark found at gene promoters and CpG islands. H3K4me3 is essential for mammalian development, yet mechanisms underlying its genomic targeting are poorly understood. H3K4me3 methyltransferases SETD1B and MLL2 are essential for oogenesis. We investigated changes in H3K4me3 in Setd1b conditional knockout (cKO) oocytes using ultra-low input ChIP-seq, with comparisons to DNA methylation and gene expression analyses. H3K4me3 was redistributed in Setd1b cKO oocytes showing losses at active gene promoters associated with downregulated gene expression. Remarkably, many regions also gained H3K4me3, in particular those that were DNA hypomethylated, transcriptionally inactive and CpG-rich, which are hallmarks of MLL2 targets. Consequently, loss of SETD1B disrupts the balance between MLL2 and de novo DNA methyltransferases in determining the epigenetic landscape during oogenesis. Our work reveals two distinct, complementary mechanisms of genomic targeting of H3K4me3 in oogenesis, with SETD1B linked to gene expression and MLL2 to CpG content. Graphical AbstractIn oogenesis, SETD1B and CXXC1 target H3K4me3 to actively transcribed gene promoters, while MLL2 targets transcriptionally inactive regions based on underlying CpG composition (upper panel). When SETD1B is ablated, H3K4me3 is lost at a subset of active promoters, resulting in downregulation of transcription (lower panel). Loss of SETD1B alters the activity of MLL2, permitting MLL2 to deposit H3K4me3 at CpG-rich regions, many of which should otherwise be DNA methylated. Thus, it is evident that MLL2 and de novo DNMTs compete for genomic occupancy late in oogenesis, and loss of SETD1B disrupts the balance of these mechanisms. O_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY

developmental biology↗

MLL1 is required for maintenance of intestinal stem cells and the expression of the cell adhesion molecule JAML

Epigenetic control is crucial for lineage-specific gene expression that creates cellular identity during mammalian development and in adult organism. Histone 3 lysine 4 methylation (H3K4) is a universal epigenetic mark. Mixed lineage leukemia (MLL1) is the founding member of the mammalian family of H3K4 methyltransferases. It was originally discovered as the main gene mutated in early onset leukemias and then found to be required for hematopoietic stem cell development and maintenance. However, the roles of MLL1 in non-hematopoietic tissues remain largely unexplored. To bypass hematopoietic lethality, we used bone marrow transplantation and conditional mutagenesis to discover that the most overt phenotype in Mll1-mutant mice is intestinal failure. Loss of MLL1 is accompanied by a differentiation bias towards the secretory lineage with increased numbers of goblet cells. MLL1 is expressed in intestinal stem cells (ISCs) and transit amplifying (TA) cells but at reduced levels in Paneth cells and not in the villus. MLL1 is required for the maintenance of intestinal stem cells (ISCs) and proliferation in the crypt. Transcriptome analysis implicate MLL1-dependent expression in ISCs of several transcription factors including Pitx2, Gata4, Foxa1 and Onecut2, and also a cell adhesion molecule, Jaml. Reactive transcriptome changes in Paneth cells and organoids imply that JAML plays a key role in the crypt stem cell niche. All known postnatal functions of MLL1 relate to stem cell maintenance and lineage decisions thereby highlighting the suggestion that MLL1 is a master stem cell regulator. Author SummaryThe ability of adult stem cells to produce functional progenies through differentiation is critical to maintain function and integrity of organs. A fundamental challenge is to identify factors that control the transition from self-renewal to the differentiated state. Epigenetic factors amongst others can fullfill such a role. Methylation of histone 3 on lysine 4 (H3K4) is a posttranslational epigenetic modification that is associated with actively transcribed genes. In mammals, this epigenetic mark is catalyzed by one of six H3K4 methyltransferases, including the founding member of the family, MLL1. MLL1 is important for the precise functioning of the hematopoietic stem cell compartment. This raises the possibility of similar functions in other adult stem cell compartments. Due to its intense self-renewal kinetics and its simple repetitive architecture, the intestinal epithelium serves as a prime model for studying adult stem cells. We demonstrate that MLL1 controls intestinal stem cell proliferation and differentiation. Additionally, transcriptome analysis suggests a pertubation in the close interaction between intestinal stem cells and neighbouring Paneth cells through loss of junction adhesion molecule like (JAML). Our work sheds new light on the function of MLL1 for the control of intestinal stem cell identity.

genetics↗

SETD1B controls cognitive function via cell type specific regulation of neuronal identity genes

Histone-3-lysine-4-methylation (H3K4me) is mediated by six different lysine methyltransferases (KMTs). Amongst these enzymes SET domain containing 1b (SETD1B) has been linked to intellectual disability but its role in the adult brain has not been studied yet. Here we show that mice lacking Setd1b from excitatory neurons of the adult forebrain exhibit severe memory impairment. By combining neuron-specific ChIP-seq, RNA-seq and single cell RNA-seq approaches we show that Setd1b controls the expression of neuronal-identity genes with a broad H3K4me3 peak linked to learning and memory processes. Our data furthermore suggest that basal neuronal gene-expression is ensured by other H3K4 KMTs such as Kmt2a and Kmt2b while the additional presence of Setd1b at the single cell level provides transcriptional consistency to the expression of genes important for learning & memory.

neuroscience↗

MLL4 is required for the first embryonic collective cell migration whereas MLL3 is not required until birth

Methylation of histone 3 lysine 4 (H3K4) is a major epigenetic system associated with gene expression. In mammals there are six H3K4 methyltransferases related to yeast Set1 and fly Trithorax, including two orthologs of fly Trithorax-related: MLL3 and MLL4. Exome sequencing has documented high frequencies of Mll3 and Mll4 mutations in many types of human cancer. Despite this emerging importance, the requirements of these sister genes in mammalian development have only been incompletely reported. Here we examined the null phenotypes to establish that MLL3 is first required for lung maturation whereas MLL4 is first required for migration of the anterior visceral endoderm (AVE) that initiates gastrulation and is the first collective cell migration in development. This migration is preceded by a columnar to squamous transition in visceral endoderm cells that depends on MLL4. Furthermore, Mll4 mutants display incompletely penetrant, sex distorted, embryonic haploinsufficiency and adult heterozygous mutants show aspects of Kabuki syndrome, indicating that MLL4 action, unlike MLL3, is dosage dependent. The highly specific and discordant functions of these sister genes argues against their action as general enhancer factors. Summary statementThe H3K4 methyltransferases MLL3 and MLL4 have strikingly different null phenotypes during mouse development; MLL3 is required for lung maturation whereas MLL4 is required for anterior visceral endoderm migration.

developmental biology↗