WormQTL2: an interactive platform for systems genetics in<i>Caenorhabditis elegans</i>

Snoek, Basten L.; Sterken, Mark G.; Hartanto, Margi; Zuilichem, Albert-Jan van; Kammenga, J.E.; Ridder, Dick de; Nijveen, Harm

doi:10.1101/766386

Cited by 16 publications

(37 citation statements)

References 131 publications

(236 reference statements)

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“…The eQTL data from the RILs were obtained from a previous publication (S noek et al 2017) and can be explored at www.bioinformatics.nl/wormqtl2 (S noek et al 2019). In short, eQTL were mapped using a single marker model, which was conducted separately for each environment.…”

Section: Methodsmentioning

confidence: 99%

Dissecting the eQTL micro-architecture inCaenorhabditis elegans

Sterken

Bevers

Volkers

et al. 2019

Preprint

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The study of expression quantitative trait loci (eQTL) using natural variation in inbred populations has yielded detailed information about the transcriptional regulation of complex traits. Studies on eQTL using recombinant inbred lines (RILs) led to insights on local and distant regulatory loci of transcript abundance. However, determining the underlying causal polymorphic genes or variants is difficult, but ultimately essential for the understanding of regulatory networks of complex traits. This requires insight into whether associated loci are single eQTL or a combination of closely linked eQTL, and how this QTL micro-architecture depends on the environment. We addressed these questions by mapping eQTL in N2 x CB4856 C. elegans RIL populations across three different environments (control, heat-stress, and recovery). To test for independent replication of the RIL eQTL, we used introgression lines (ILs). Both populations indicate that the overall heritability, number, and position of eQTL differed among environments. Across environments we were able to replicate 70% of the local- and 40% of the distant-eQTL using the ILs. Simulation models revealed that additive effects explain up to 60-93% of RIL/IL heritability across environments. Closely linked eQTL explained up to 40% of RIL/IL heritability in the control environment whereas only 7% in the heat-stress and recovery environments. In conclusion, we show that reproducibility of eQTL was higher for local vs. distant eQTL and that the environment affects the eQTL micro-architecture.

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Section: Methodsmentioning

confidence: 99%

Dissecting the eQTL micro-architecture inCaenorhabditis elegans

Sterken

Bevers

Volkers

et al. 2019

Preprint

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“…The eQTL data from the RILs were obtained from a previous publication (Snoek et al, 2017) and can be explored at www.bioinformatics.nl/wormqtl2 (Snoek et al, 2020). In short, previously eQTL were mapped using a single marker model, which was conducted separately for each environment.…”

Section: Eqtl Datamentioning

confidence: 99%

Dissecting the eQTL Micro-Architecture in Caenorhabditis elegans

et al. 2020

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The study of expression quantitative trait loci (eQTL) using natural variation in inbred populations has yielded detailed information about the transcriptional regulation of complex traits. Studies on eQTL using recombinant inbred lines (RILs) led to insights on cis and trans regulatory loci of transcript abundance. However, determining the underlying causal polymorphic genes or variants is difficult, but ultimately essential for the understanding of regulatory networks of complex traits. This requires insight into whether associated loci are single eQTL or a combination of closely linked eQTL, and how this QTL micro-architecture depends on the environment. We addressed these questions by testing for independent replication of previously mapped eQTL in Caenorhabditis elegans using new data from introgression lines (ILs). Both populations indicate that the overall heritability of gene expression, number, and position of eQTL differed among environments. Across environments we were able to replicate 70% of the cis-and 40% of the trans-eQTL using the ILs. Testing eight different simulation models, we suggest that additive effects explain up to 60-93% of RIL/IL heritability for all three environments. Closely linked eQTL explained up to 40% of RIL/IL heritability in the control environment whereas only 7% in the heat-stress and recovery environments. In conclusion, we show that reproducibility of eQTL was higher for cis vs. trans eQTL and that the environment affects the eQTL micro-architecture.

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“…The eQTL data was mined from http://www.bioinformatics.nl/EleQTL [69]. mock, N2 infected, CB4856 mock and CB856 infected conditions.…”

Section: Eqtl Data Analysismentioning

confidence: 99%

Balancing selection of the Intracellular Pathogen Response in natural Caenorhabditis elegans populations

Sluijs

Bosman

Pankok

et al. 2019

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23 0031317482998 24 Mark.Sterken@wur.nl 25 Our work provides evidence that balancing genetic selection shapes the transcriptional defence against pathogens 48 in C. elegans. The transcriptional and genetic data in this study demonstrate the functional diversity that can 49 develop within antiviral transcriptional responses in natural host populations. 50 Page 3 of 28 Background 51 The continuous battle between host and virus drives host genetic variation to arise in antiviral mechanisms such 52 as transcriptional responses. Regulatory genetic variation affects the viral susceptibility after infection, making 53 some individuals within the population more resistant than others [1-4]. Yet, the universality and mode-of-action 54 of genetic diversity in shaping antiviral transcriptional responses within natural populations remains largely 55 unknown. 56 Caenorhabditis elegans and its natural pathogen Orsay virus (OrV) are used as a powerful genetic 57 model system to study host-virus interactions [5]. OrV is a positive-sense single-stranded RNA virus infecting C. 58 elegans intestinal cells where it causes local disruptions of the cellular structures [5, 6]. Two major groups of 59 antiviral genes respond to viral infection in C. elegans: genes related to the RNA interference (RNAi) pathway 60 [5, 7-12] and genes related to the Intracellular Pathogen Response (IPR) [13-16]. The RNAi pathway activity is 61 controlled by the gene sta-1 which in turn is activated by the viral sensor sid-3 that is hypothesized to directly 62 interact with the Orsay virus [7]. Subsequently, the antiviral RNAi components dcr-1, drh-1, and rde-1 degrade 63 the viral RNA [9], but the RNAi genes themselves remain equally expressed during infection [9, 16]. The IPR 64 counteracts infection by intracellular pathogens (including OrV) and increases the ability to handle proteotoxic 65 stress [13-15]. The gene pals-22 co-operates together with pals-25 to control the IPR pathway by functioning as 66 a molecular switch between growth and antiviral defence. Pals-22 promotes development and lifespan, whereas 67 pals-25 stimulates pathogen resistance. Together pals-22 and pals-25 regulate a set of 80 genes that are 68 upregulated upon intracellular infection including 25 genes in the pals-family and several members of the 69 ubiquitination response [14, 15].. Both pals-22 and pals-25 do not change gene expression following OrV 70 infection. In total, the pals-gene family contains 39 members mostly found in five genetic clusters on 71 chromosome I, III, and V.. Recently, a third antiviral defence was identified which degrades the viral genome 72 after uridylation by the gene cde-1 [17]. Together, these antiviral pathways are key in controlling OrV infection 73 in C. elegans. 74The transcriptional responses following infection have so far been studied in the C. elegans laboratory 75 strain N2, in RNAi deficient mutants in the N2 background such as rde-1 and dcr-1 and in the RNAi-deficient 76 wild isolate JU1580 [7, 9, 10, 13, 14, 16]. These studies indica...

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WormQTL2: an interactive platform for systems genetics inCaenorhabditis elegans

Cited by 16 publications

References 131 publications

Dissecting the eQTL micro-architecture inCaenorhabditis elegans

Dissecting the eQTL micro-architecture inCaenorhabditis elegans

Dissecting the eQTL Micro-Architecture in Caenorhabditis elegans

Balancing selection of the Intracellular Pathogen Response in natural Caenorhabditis elegans populations

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