Biology subjects

Moore, N. A.

Publications and source records attributed to Moore, N. A..

3 recordsLinked to original sources

bioRxiv2026

Dispersal rate limits range expansion rate only when it is slower than climate velocity

Low dispersal ability might limit a species capacity to track its climate preferences across the landscape, yet evidence that low dispersal slows species range shifts under contemporary climate change remains contentious. Here we develop a new hypothesis under which we expect variation in dispersal ability to affect range expansion rates only when climate velocity exceeds dispersal rates, which is logical yet rarely applied because it requires a common yardstick to compare rates. We test this hypothesis using empirical relationships between dispersal ability, local range expansion rate, and the velocity of isotherm shifts in terrestrial plants and birds, all estimated in km/yr. In 370 range shifts, we found that range expansion rates were best explained by the slower of either a species dispersal rate or the velocity of isotherm shifts, as predicted under our hypothesis. Furthermore, when species dispersal rates were slower than the velocity of isotherm shifts, we found that dispersal ability positively affects range shift rates. Substantial variation in range expansion rates remained unexplained, indicating that additional factors influence range shift dynamics. Our results provide new clarity when understanding the role of dispersal ability on variation in range shift rates and emphasize the importance of evaluating dispersal capacity relative to climatic change exposure when testing hypotheses about species responses to ongoing environmental change. Significance StatementSpecies dispersal ability is widely thought to limit biodiversity redistribution in response to climate change, but we still lack a clear understanding of when or for which species dispersal limitations matter. Using hundreds of range expansion rates documented over the 10 last decades for terrestrial birds and plants together with their dispersal rates, in common units of km/yr, we show that dispersal ability slows climate-mediated range expansion, but that dispersal limitations occur only when the rates of climate change are faster than the ability of species to redistribute. So far, many species display dispersal rates higher than the velocity of climate change but dispersal limitations may become more pronounced in the future.

ecology↗

bioRxiv2023

Unveiling APOL1 Haplotypes: A Novel Classification Through Probe-Independent Quantitative Real-Time PCR

IntroductionApolipoprotein-L1 (APOL1) is a primate-specific protein component of high- density lipoprotein (HDL). Two variants of APOL1 (G1 and G2), provide resistance to parasitic infections in African Americans but are also implicated in kidney-related diseases and transplant outcomes in recipients. This study aims to identify these risk variants using a novel probe- independent quantitative real-time PCR method in a high African American recipient cohort. Additionally, it aims to develop a new stratification approach based on haplotype-centric model. MethodsGenomic DNA was extracted from recipient PBMCs using SDS lysis buffer and proteinase K. Quantitative PCR assay with modified forward primers and a common reverse primer enabled us to identify single nucleotide polymorphisms (SNPs) and the 6-bp deletion quantitatively. Additionally, we used sanger sequencing to verify our QPCR findings. ResultsOur novel probe-independent qPCR effectively distinguished homozygous wild-type, heterozygous SNPs/deletion, and homozygous SNPs/deletion, with at least 4-fold differences. High prevalence of APOL1 variants was observed (18% two-risk alleles, 34% one-risk allele) in our recipient cohort. Intriguingly, up to 12-month follow-up revealed no significant impact of recipient APOL1 variants on transplant outcomes. Ongoing research will encompass more time points and a larger patient cohort, allowing a comprehensive evaluation of G1/G2 variant subgroups categorized by new haplotype scores, enriching our understanding. ConclusionsOur cost-effective and rapid qPCR technique facilitates APOL1 genotyping within hours. Prospective and retrospective studies will enable comparisons with long-term allograft rejection, potentially predicting early/late-stage transplant outcomes based on haplotype evaluation in this diverse group of kidney transplant recipients.

genetics↗

bioRxiv2018

Activation of the unfolded protein response and inhibition of translation initiation during coronavirus infection

Coronavirus infection induces the unfolded protein response (UPR), a cellular signalling pathway composed of three branches, triggered by unfolded proteins in the endoplasmic reticulum (ER) due to high ER load. We have used RNA sequencing and ribosome profiling to investigate holistically the transcriptional and translational response to cellular infection by murine hepatitis virus (MHV), often used as a model for the Betacoronavirus genus to which the recently emerged SARS-CoV-2 also belongs. We found the UPR to be amongst the most significantly up-regulated pathways in response to MHV infection. To confirm and extend these observations, we show experimentally the induction of all three branches of the UPR in both MHV- and SARS-CoV-2-infected cells. Over-expression of the SARS-CoV-2 ORF8 or S proteins alone is itself sufficient to induce the UPR. Remarkably, pharmacological inhibition of the UPR greatly reduced the replication of both MHV and SARS-CoV-2, revealing the importance of this pathway for successful coronavirus replication. This was particularly striking when both IRE1 and ATF6 branches of the UPR were inhibited, reducing SARS-CoV-2 virion release [~]1,000-fold. Together, these data highlight the UPR as a promising antiviral target to combat coronavirus infection. Author SummarySARS-CoV-2 is the novel coronavirus responsible for the COVID-19 pandemic which has resulted in over 100 million cases since the end of 2019. Most people infected with the virus will experience mild to moderate respiratory illness and recover without any special treatment. However, older people, and those with underlying medical problems like chronic respiratory disease are more likely to develop a serious illness. So far, more than 2 million people have died of COVID-19. Unfortunately, there is no specific medication for this viral disease. In order to produce viral proteins and to replicate their genetic information, all coronaviruses use a cellular structure known as the endoplasmic reticulum or ER. However, the massive production and modification of viral proteins stresses the ER and this activates a compensatory cellular response that tries to reduce ER protein levels. This is termed the unfolded protein response or UPR. We believe that coronaviruses take advantage of the activation of the UPR to enhance their replication. The UPR is also activated in some types of cancer and neurodegenerative disorders and UPR inhibitor drugs have been developed to tackle these diseases. In this work, we have tested some of these compounds in human lung cells infected with SARS-CoV-2 and found that virus production was reduced 1000-fold in human lung cells.

microbiology↗