Emma, M. | bioRxiv Science

bioRxiv2026

AN UPDATED POPULATION ESTIMATE FOR NORTHERN GANNETS ACROSS THEIR NORTH-EAST ATLANTIC BREEDING RANGE FOLLOWING THE 2022 OUTBREAK OF HIGH PATHOGENICITY AVIAN INFLUENZA

Northern gannets (Morus bassanus) have been regarded as a seabird success story, due to population increases throughout the 20th and 21st century contrasting with global seabird declines. However, in 2022 gannets experienced a severe outbreak of High Pathogenicity Avian Influenza (HPAI) across their global distribution, leading to an urgent need to reassess their population status. This study presents breeding gannet census numbers for 2023/24 from all colonies across the North-East Atlantic metapopulation (Great Britain, Ireland, the Channel Islands, Iceland, Norway, the Faroe Islands, France, Germany, Russia). Gannet numbers decreased by 17% across the North-East Atlantic metapopulation between the 2013/14 and 2023/24 census from 414,598 to 345,854 apparently occupied sites (AOS), a global decrease of at least 13%. The bulk of the reduction in AOS was driven by the largest colonies (>10,000 AOS) each losing tens of thousands of AOS. These figures likely underestimate the impact of the HPAI outbreak worldwide, since most colonies will have increased between the last census in 2013/14 and the 2022 HPAI outbreak, and the Canadian breeding population was last counted pre-HPAI outbreak. Scotland still holds the largest proportion of both the North-East Atlantic metapopulation (59%), and the world population (46%), while Great Britain, Ireland and the Channel Islands together hold 83% of the North-East Atlantic metapopulation and 64% of the world population. This study not only presents an updated population census for gannets in the North-East Atlantic but illustrates the large-scale impacts of a disease outbreak on a seabird species across its global range and highlights the importance of more regular census efforts to better quantify the demographic consequences of such events.

ecology↗

bioRxiv2024

Complete telomere-to-telomere assemblies of two sorghum genomes to guide biological discovery

Sorghum is a C4 crop well-known for its high efficiency of biomass accumulation and adaptation to drought and hot environments. This study reports the assembly of complete genome sequence of two sorghum genomes using a combination of ultra-long reads from Oxford Nanopore Technology, high-fidelity long reads from Pacbio and Hi-C reads. The accuracy and completeness of the T2T assemblies were comprehensively validated using a range of parameters, including coverage depth assessment, BUSCO, LTR assembly index, ect. Our T2T assembly of BTx623 identified 36.25 Mb of new sequence, in addition to dozens of misoritation and mispositioning of large DNA segments in the BTx623-v3. Correcting these assembly errors in the reference genome is critical for exploiting genetic information in these complex regions in sorghum. Comparison of the two T2T genomes shed new insights on variation of centromeres in sorghum. The two high-quality T2T genomes represent an important resource for sorghum improvement and gene discovery. They would serve as the new reference genomes to unlock the full potential of global sequence variation of this valuable crop.

genomics↗

bioRxiv2020

NUPR1 protects liver from lipotoxic injury by improving the endoplasmic reticulum stress response

Background and AimsNon-alcoholic fatty liver disease and related hepatic syndromes affect up to one third of the adult population. The molecular mechanisms underlying NAFL etiology remain elusive. Nuclear Protein 1 (NUPR1) expression increases upon cell injury in all organs and recently we report its active participation in the activation of the Unfolded Protein Response (UPR). The UPR typically maintains protein homeostasis, but downstream mediators of the pathway regulate metabolic functions, including lipid metabolism. NUPR1 and UPR increase have been reported in obesity and liver pathologies and the goal of this study was to investigate the roles of NUPR1 in this context. MethodsWe used patient-derived liver biopsies and in vitro and in vivo NUPR1 loss of functions models. First, we analysed NUPR1 expression in a cohort of morbidly obese patients (MOPs), with either simple fatty liver (NAFL) or more severe steatohepatitis (NASH). Next, we explored the metabolic roles of NUPR1 in wild type (Nupr1+/+) or Nupr1 knockout mice (Nupr1-/-) fed ad libitum with a high fat diet (HFD) for up to 15 weeks. ResultsNUPR1 expression is inversely correlated to hepatic steatosis progression. We found that NUPR1 participates in the activation of PPAR- signalling via UPR. PPAR- signalling, is involved in the maintenance of fat metabolism and proper lipid homeostasis and energy balance. As PPAR- signalling is controlled by UPR, collectively, these findings suggest a novel function for NUPR1 in protecting liver from metabolic distress by controlling lipid homeostasis, possibly through the UPR. ObjectiveNon-alcoholic fatty liver (NAFL) disease and related hepatic syndromes affect up to one third of the adult population in industrialised and developing countries. However, the molecular mechanisms underlying NAFL etiology remain elusive. Nuclear Protein 1 (NUPR1) expression increases upon cell injury in all organs including the liver. Recently, we report NUPR1 actively participates in activation of the Unfolded Protein Response (UPR). The UPR typically maintains protein homeostasis, but downstream mediators of the pathway regulate metabolic functions, including lipid metabolism. NUPR1 and UPR increase have been reported in obesity and liver pathologies and the goal of this study was to investigate the roles of NUPR1 in this context. DesignWe used patient-derived liver biopsies and in vitro and in vivo NUPR1 loss of functions models. First, we analysed NUPR1 expression in a cohort of morbidly obese patients (MOPs), with either simple fatty liver (NAFL) or more severe steatohepatitis (NASH). Next, we explored the metabolic roles of NUPR1 in wild type (Nupr1+/+) or Nupr1 knockout mice (Nupr1-/-) fed ad libitum with a high fat diet (HFD) for up to 15 weeks. ResultsNUPR1 expression is inversely correlated to hepatic steatosis progression. Mechanistically, we found NUPR1 participates in the activation of PPAR- signalling via UPR. PPAR- signalling, is involved in the maintenance of fat metabolism and proper lipid homeostasis and energy balance. As PPAR- signalling is controlled by UPR, collectively, these findings suggest a novel function for NUPR1 in protecting liver from metabolic distress by controlling lipid homeostasis, possibly through the UPR. ConclusionsAs PPAR- signalling is controlled by UPR, collectively, these findings suggest a novel function for NUPR1 in protecting liver from metabolic distress by controlling lipid homeostasis, possibly through the UPR. Lay summaryNUPR1 is activated during high caloric intake in both mice and patients. Decrease in expression or inhibition of NUPR1 worsens lipid deposition and hepatic damage. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=192 SRC="FIGDIR/small/350652v1_ufig1.gif" ALT="Figure 1"> View larger version (46K): org.highwire.dtl.DTLVardef@1d370c0org.highwire.dtl.DTLVardef@8f8dc9org.highwire.dtl.DTLVardef@a5aa49org.highwire.dtl.DTLVardef@4eb585_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LINUPR1 protects liver from high caloric intake hepatic damage C_LIO_LIThe function of NUPR1 in this context is to control the lipid homeostasis through the UPR and more specifically through PPAR- signalling. C_LIO_LINUPR1 could be used as a predictive marker for the gravity of NAFL progression. Moreover, as clinical interest is being raised around NUPR1 inhibitors to treat liver and pancreatic cancer, care should be taken in monitoring lipotoxic parameters. C_LI

cell biology↗