Biology subjects

Mitchell, K. A.

Publications and source records attributed to Mitchell, K. A..

6 recordsLinked to original sources

bioRxiv2026

Description of Venenivibrio orakeikorakoensis sp. nov. and Venenivibrio aotearoaensis sp. nov, and emended description of genus Venenivibrio, Venenivibrio stagnispumantis species

Two thermophilic bacterial strains, designated OKO1 and KUI1, were isolated from hot springs within the Taup[o] Volcanic Zone of New Zealand. Analysis of the 16S rRNA gene identified both as members of the genus Venenivibrio, sharing 99.13% and 98.82% sequence similarity with Venenivibrio stagnispumantis CP.B2T, respectively. The novel isolates were characterised using a polyphasic taxonomic approach alongside V. stagnispumantis. Despite their close phylogenetic relationship, the strains differed markedly in cell morphology, physiology and genomic content. Both isolates exhibited broad tolerance to temperature and pH, while re-examination V. stagnispumantis CP.B2T revealed substantially wider physiological capabilities than previously reported, bringing its phenotype into closer agreement with the new isolates. Comparative genomic analyses identified key differences in genes encoding cytochromes, hydrogenases, and nitrogen metabolism, suggesting distinct metabolic potential among the strains. Although the genomes shared average nucleotide identity (ANI) values of 95-96%, placing them near the accepted species boundary, the combined phenotypic and genomic evidence support recognition of OKO1T and KUI1T as two species within the genus. We therefore propose Venenivibrio orakeikorakoensis sp. nov. (type strain OKO1T, ACCESSION) and Venenivibrio aotearoaensis sp. nov. (type strain KUI1T, ACCESSION) as new members within the genus, and emend the descriptions of Venenivibrio stagnispumantis and the genus Venenivibrio to incorporate the expanded phenotypic and genomic diversity revealed in this study.

microbiology↗

bioRxiv2026

Reysenbachia aerophila gen. nov., sp. nov., a facultatively anaerobic, hydrogen-oxidizing, thermophilic bacterium isolated from Kuirau Park, Rotorua, New Zealand

A facultatively anaerobic, hydrogen-oxidizing, thermophilic bacterium (strain KUI-RBT) was isolated from a geothermal spring biofilm in Rotorua, New Zealand. Strain KUI-RBT is a motile, straight rod, measuring approximately 0.7 {micro}m by 1.0 to 1.5 {micro}m with a diderm cell wall. Growth of KUI-RBT occurred from 39 to 74 {degrees}C (Topt 64.5 {degrees}C), pH 5.0 to 7.5 (pHopt 6.5), and 0 to 1% (w/v) NaCl (NaClopt 0.4-0.7%, w/v). KUI-RBT utilizes carbon dioxide and various organic carbon substrates as carbon sources and hydrogen as an electron donor. KUI-RBT can use oxygen (0-21%, v/v), elemental sulfur, thiosulfate, sulfite, nitrate, arsenate, and selenate as terminal electron acceptors. Major fatty acids of strain KUI-RBT include C20:1, C18:1, and C18:0 and the primary quinone is MTK-7. The whole genome G+C content is 34.23 mol%. Phylogenetic analyses indicate KUI-RBT to be a member of the family Hydrogenothermaceae, with Sulfurihydrogenibium azorense Az-Fu1T its closest characterised relative (94.51% 16S rRNA gene sequence similarity, 78.01% whole genome ANI, 61.34% whole genome AAI). Based on phylogenetic and phenotypic analyses, we propose KUI-RBT represents a novel genus and species within the family Hydrogenothermaceae, for which we propose the name Reysenbachia aerophila gen. nov., sp. nov. The type strain is KUI-RBT (=KCTC accession =JCM accession). The GenBank accession number for the 16S rRNA gene sequence of strain KUI-RBT is PZ052650. The GenBank accession number for the whole genome of strain KUI-RBT is JBVODP000000000.

microbiology↗

bioRxiv2026

Hippo pathway perturbation disrupts cell fate control in the Drosophila eye

During animal development, cells acquire specialised fates in a precise spatiotemporal order, which is essential for producing tissues that function appropriately. Cell fate specification is governed by multiple signalling pathways, as well as mechanical forces, which impact cellular transcription. Two such signalling pathways are the Hippo pathway and EGFR pathway, which both control organ growth and the fate of certain cell types in multiple species. Here, we show that Hippo signalling is essential for the maintenance of the cone and primary pigment cell fates in the developing Drosophila eye. When Hippo signalling is compromised, its nuclear effectors Yorkie and Scalloped drive increased expression of the EGFR pathway transcription repressor Yan, which antagonises the cone and primary pigment cell fates. Thus, in addition to its role as a growth suppressor, Hippo signalling promotes the fate of multiple eye cells by maintaining their responsiveness to inductive cues from the EGFR pathway. AUTHOR SUMMARYAs multicellular organisms grow and develop from a zygote, individual cells become increasingly specialised. Cell fate is specified and maintained by the coordinate action of different signalling pathways, whose activity must be tightly controlled in a spatiotemporal fashion. If this fails, cell fate can be disturbed, which can cause developmental abnormalities, and diseases such as cancers. Here, we describe a new function for the Hippo signalling pathway, which was originally discovered as a regulator of Drosophila tissue growth and subsequently linked to the genesis of multiple human cancers. Hippo signalling is essential for maintaining the fate of two key cell types in the Drosophila eye, primary pigment cells and cone cells. Without Hippo signalling these cells cannot properly respond to signals from another key signalling network, the EGFR pathway. Our discoveries add to a growing literature where the Hippo growth control pathway is repurposed to control cell fate in tissues that have ceased growth.

developmental biology↗

bioRxiv2024

Damsel: Analysis and visualisation of DamID sequencing in R

SummaryDamID sequencing is a technique to map the genome-wide interaction of a protein with DNA. Damsel is the first Bioconductor package to provide an end to end analysis for DamID sequencing data within R. Damsel performs quantification and testing of significant binding sites along with exploratory and visual analysis. Damsel produces results consistent with previous analysis approaches. Availability and implementationThe R package Damsel is available for install through the Bioconductor project https://bioconductor.org/packages/release/bioc/html/Damsel.html and the code is available on GitHub https://github.com/Oshlack/Damsel/ Contactcaitlin.page@petermac.org Supplementary informationAvailable through the journal.

bioinformatics↗

bioRxiv2024

GM-CSF-mediated epithelial-immune cell crosstalk orchestrates pulmonary immunity to Aspergillus fumigatus

Aspergillus fumigatus causes life-threatening mold pneumonia in immune compromised patients, particularly in those with quantitative or qualitative defects in neutrophils. While innate immune cell crosstalk licenses neutrophil antifungal activity in the lung, the role of epithelial cells in this process is unknown. Here, we find that that surfactant protein C (SPC)-expressing lung epithelial cells integrate infection-induced IL-1 and type III interferon signaling to produce granulocyte-macrophage colony-stimulating factor (GM-CSF) preferentially at local sites of fungal infection and neutrophil influx. Using in vivo models that distinguish the role of GM-CSF during acute infection from its homeostatic function in alveolar macrophage survival and surfactant catabolism, we demonstrate that epithelial-derived GM-CSF increases the accumulation and fungicidal activity of GM-CSF-responsive neutrophils, with the latter being essential for host survival. Our findings establish SPC+ epithelial cells as a central player in regulating the quality and strength of neutrophil-dependent immunity against inhaled mold pathogens. HIGHLIGHTSO_LIGM-CSF is essential for host defense against A. fumigatus in the lung C_LIO_LIIL-1 and IFN-{lambda} promote GM-CSF production by lung epithelial cells in parallel C_LIO_LIEpithelial cell-derived GM-CSF increases neutrophil accumulation and fungal killing capacity C_LIO_LIEpithelial cells preferentially upregulate GM-CSF in local sites of inflammation C_LI GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=128 SRC="FIGDIR/small/574062v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@708497org.highwire.dtl.DTLVardef@11106f7org.highwire.dtl.DTLVardef@e08140org.highwire.dtl.DTLVardef@1459e89_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2019

Higher prevalence of homologous recombination-deficiency in lung squamous carcinoma from African Americans

To improve our understanding of the longstanding disparities in incidence and mortality across multiple cancer types among minority populations, we performed a systematic comparative analysis of molecular features in tumors from African American (AA) and European American (EA) ancestry. Our pan-cancer analysis on the cancer genome atlas (TCGA) and a more focused analysis of genome-wide somatic copy number profiles integrated with tumor-normal RNA sequencing in a racially balanced cohort of 222 non-small cell lung cancers (NSCLC) reveals more aggressive genomic characteristics of AA tumors. In general, we find AA tumors exhibit higher genomic instability (GI), homologous recombination-deficiency (HRD) levels, and more aggressive molecular features such as chromothripsis across many cancer types, including lung squamous carcinoma (LUSC). GI and HRD levels are strongly correlated across AA tumors, indicating that HRD plays an important role in GI in these patients. The prevalence of germline HRD is higher in AA tumors, suggesting that the somatic differences observed have genetic ancestry origins. Finally, we identify AA-specific copy number-based arm, focal and gene level recurrent features in lung cancer, including a higher frequency of PTEN deletion and KRAS amplification and a lower frequency of CDKN2A deletion. These results highlight the importance of including minority and under-represented populations in genomics research and may have therapeutic implications.

cancer biology↗