14 research outputs found

    Climate change is associated with asynchrony in arrival between two sympatric cuckoos and both host arrival and prey emergence

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    Matching the timing of spring arrival to the breeding grounds with hosts and prey is crucial for migratory brood parasites such as cuckoos. Previous studies have focused mostly on phenological mismatch between a single cuckoo species and its hosts but information regarding climate-driven mismatch between multiple sympatric cuckoo species and their hosts and invertebrate prey is still lacking. Here, we analysed long-term data (1988–2023) on the first arrival date of two declining migratory cuckoo species and their 14 migratory host species breeding in sympatry and prey emergence date in Tatarstan (southeast Russia). We found that the common cuckoo (Cuculus canorus; wintering in Africa) generally arrived on breeding grounds earlier than the oriental cuckoo (Cuculus optatus; wintering in southeast Asia and Australia). Both cuckoos have advanced their arrival dates over 36 years but less than their hosts, potentially resulting in an increasing arrival mismatch between cuckoos and their hosts. Moreover, cuckoo arrival advanced less than the emergence date of their prey over time. These observations indicate that climate change may disrupt co-fluctuation in the phenology of important life stages between multiple sympatric brood parasites, their hosts and prey with potential cascading consequences for population dynamics of involved species

    Synchronous Recruitment of Epigenetic Modifiers to Endotoxin Synergistically Activated Tnf-α Gene in Acute Kidney Injury

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    <div><p>Background</p><p>As a consequence of acute kidney injury (AKI), proximal tubular cells hyperrespond to endotoxin (lipopolysaccharide, LPS) by exaggerated renal Tnf-α Production. This LPS hyperresponsiveness is transcriptionally mediated. The epigenetic pathways that control these responses are unknown.</p><p>Methods/Findings</p><p>We applied multiplex chromatin immunoprecipitation platform (Matrix ChIP) to explore epigenetic pathways that underlie endotoxin hyperresponsiveness in the setting of preceding unilateral renal ischemia/reperfusion (I/R) in mouse AKI model. Endotoxin exposure after I/R resulted in enhanced transcription, manifested by hyperresponsive recruitment of RNA polymerase II (Pol II) at the Tnf-α gene. At this locus, LPS but not I/R increased levels of Pol II C-terminal domain (CTD) phosho-serine2 &5 and induced dephosphorylation of the transcription-repressive histone H4 phospho-serine-1. In contrast, I/R but not LPS increased the transcription-permissive histone phosphorylation (H3 phospho-serine-10, H3.3 phospho-serine-31) at the Tnf-α gene. In agreement with these observations, I/R but not LPS increased activity of cognate kinases (Erk1/2, Msk1/2 and Aurora A) at the Tnf-α locus. Cross-talk of histone phosphorylation and acetylation synergize to active gene expression. I/R and LPS increased histone acetylation. (H3K9/14Ac, H4K5/8/12/16Ac, H2KA5Ac, H2BK4/7Ac). Levels of some histone acetyltransferases at this gene (PCAF and MOF) were increased by I/R but not by LPS, while others were induced by either I/R or LPS and exhibited endotoxin hyperresponsive patterns (GCN5, CBP and p300). The adaptor protein 14-3-3 couples histone phosphorylation with acetylation, and tethers chromatin modifiers/transcription elongation factors to target genes. Both I/R and LPS increased levels of 14-3-3 and several chromatin/transcription modifiers (BRD4, BRG1, HP-1γ and IKKα) at the Tnf-α gene, all exhibiting endotoxin hyperresponsive recruitment patterns similar to Pol II.</p><p>Conclusions</p><p>Our results suggest that I/R and LPS differentially trigger phosphorylation (Pol II and histone) and acetylation (histone) epigenetic pathways that interact at the Tnf-α gene to generate endotoxin hyperresponse in AKI.</p></div

    Supplementary Information from Climate change is associated with asynchrony in arrival between two sympatric cuckoos and both host arrival and prey emergence

    No full text
    Matching the timing of spring arrival to the breeding grounds with hosts and prey is crucial for migratory brood parasites such as cuckoos. Previous studies have focused mostly on phenological mismatch between a single cuckoo species and its hosts but information regarding climate-driven mismatch between multiple sympatric cuckoo species and their hosts and invertebrate prey is still lacking. Here, we analysed long-term data (1988–2023) on the first arrival date of two declining migratory cuckoo species and their 14 migratory host species breeding in sympatry and prey emergence date in Tatarstan (southeast Russia). We found that the common cuckoo (Cuculus canorus; wintering in Africa) generally arrived on breeding grounds earlier than the oriental cuckoo (Cuculus optatus; wintering in southeast Asia and Australia). Both cuckoos have advanced their arrival dates over 36 years but less than their hosts, potentially resulting in an increasing arrival mismatch between cuckoos and their hosts. Moreover, cuckoo arrival advanced less than the emergence date of their prey over time. These observations indicate that climate change may disrupt co-fluctuation in the phenology of important life stages between multiple sympatric brood parasites, their hosts and prey with potential cascading consequences for population dynamics of involved species

    Matrix ChIP analysis of permissive histone acetylation marks at and <i>Tnf-α</i> genes following unilateral kidney I/R and LPS injection.

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    <p>Sheared cross-linked renal cortex chromatin from mice were assayed using antibodies to acetylated histones and total histone H3. ChIP DNA were analyzed at the Tnf-α first and last exon and CypA first exon first in real-time PCR. Data represent mean ± SEM (6 animals from each group), expressed as fraction of input.</p

    Matrix ChIP analysis of RNA polymerase II (Pol II) <i>Tnf-α</i> genes following unilateral kidney I/R and LPS injection.

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    <p>Sheared cross-linked renal cortex chromatin from mice were assayed using antibodies to the Pol II N-terminus and CTD modifications. ChIP DNA were analyzed at the Tnf-α first and last exon and CypA first exon in real-time PCR. Data represent mean ± SEM (6 animals from each group), expressed as fraction of input. Schematic of the genes is shown above the graphs; exons are shown as rectangles (taller and shorter rectangles represent translated and untranslated regions), lines represent introns. Black boxes shows location of the amplicon.</p

    Analysis of renal <i>Tnf-α</i> expression following unilateral kidney I/R and LPS injection.

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    <p>Total RNA from mice renal cortex was used in RT reactions with random hexamers. cDNA was used in real time PCR with gene specific primers (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070322#pone.0070322.s004" target="_blank">Table S1</a>). mRNA level of a given gene in each sample was normalized to βactin transcript. Data are represented as mean±SEM, n = 6 mice in each group.</p

    Matrix ChIP analysis of kinases at the <i>Tnf-α</i> gene following unilateral kidney I/R and LPS injection.

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    <p>Sheared cross-linked renal cortex chromatin from mice were assayed using antibodies to active (phosphorylated) and total kinases. ChIP DNA were analyzed at the Tnf-α first and last exon and CypA first exon first in real-time PCR. Data represent mean ± SEM (6 animals from each group), expressed as fraction of input.</p

    Matrix ChIP analysis of chromatin modifiers at the <i>Tnf-α</i> gene following unilateral kidney I/R and LPS injection.

    No full text
    <p>Sheared cross-linked renal cortex chromatin from mice were assayed using antibodies to chromatin modifiers. ChIP DNA were analyzed at the Tnf-α first and last exon and CypA first exon in real-time PCR. Data represent mean ± SEM (6 animals from each group), expressed as fraction of input.</p

    Matrix ChIP analysis of histone acetyltransferases at the <i>Tnf-α</i> gene following unilateral kidney I/R and LPS injection.

    No full text
    <p>Sheared cross-linked renal cortex chromatin from mice were assayed using antibodies to histone acetyltransferase. ChIP DNA were analyzed at the Tnf-α first and last exon and CypA first in real-time PCR. Data represent mean ± SEM (6 animals from each group), expressed as fraction of input.</p
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