Spatial Transcriptomics of C. elegans Males and Hermaphrodites Identifies Sex-Specific Differences in Gene Expression Patterns

Ebbing, Annabel; Vértesy, Ábel; Betist, Marco C.; Spanjaard, Bastiaan; Junker, Jan Philipp; Berezikov, Eugène; Oudenaarden, Alexander van; Korswagen, Hendrik C.

doi:10.1016/j.devcel.2018.10.016

Cited by 70 publications

(95 citation statements)

References 52 publications

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“…The transcriptome analysis of distinct cell lineages, as conducted for C. elegans precursors of endoderm, mesoderm and ectoderm (Hashimshony et al 2014) or for single-cell transcriptomes throughout embryogenesis (Hashimshony et al 2012, Tintori et al 2016, Packer et al 2019, provides one intriguing scheme for approaching this issue. Another approach could incorporate developmental time into transcriptome analysis of serial-sectioned samples to access 4-dimensional expression profiles through developmental space and time (Ebbing et al 2018).…”

Section: Modularity Of Genetic Network Architecturementioning

confidence: 99%

“…Genes also can be grouped according to patterns of co-expression to analyze for consistent differences in rates of molecular evolution among them or among parameters of mathematical functions that describe the temporal profiles of expression (Coronado-Zamora et al 2019, Cutter et al 2019. Spatial definition of expression can enhance such approaches using tissue-and sex-specificity (Kim et al 2016), restricted cell-lineages (Hashimshony et al 2014), or tomographic expression profiling (Ebbing et al 2018). While mRNA expression is most commonly accessed, all of these approaches can be extended to protein expression; protein levels appear to differ less between species than do transcriptomes (Leducq et al 2012, Khan et al 2013.…”

Section: Concentricmentioning

confidence: 99%

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Speciation and the developmental alarm clock

Cutter

Bundus

2020

Preprint

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AbstractNew species arise as the genomes of populations diverge. The developmental ‘alarm clock’ of speciation sounds off when sufficient divergence in genetic control of development leads hybrid individuals to infertility or inviability, the world awoken to the dawn of new species with intrinsic post-zygotic reproductive isolation. Some developmental stages will be more prone to hybrid dysfunction due to how molecular evolution interacts with the ontogenetic timing of gene expression. Considering the ontogeny of hybrid incompatibilities provides a profitable connection between ‘evo-devo’ and speciation genetics to better link macroevolutionary pattern, microevolutionary process, and molecular mechanisms. Here we explore speciation alongside development, emphasizing their mutual dependence on genetic network features, fitness landscapes, and developmental system drift. We assess models for how ontogenetic timing of reproductive isolation can be predictable. Experiments and theory within this synthetic perspective can help identify new rules of speciation as well as rules in the molecular evolution of development.Impact StatementIntegrating speciation genetics with ontogeny can identify predictable rules in the molecular evolution of developmental pathways and in the accumulation of reproductive isolation as genomes diverge.

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Section: Modularity Of Genetic Network Architecturementioning

confidence: 99%

Section: Concentricmentioning

confidence: 99%

Speciation and the developmental alarm clock

Cutter

Bundus

2020

Preprint

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“…Because Orsay virus infection does not infect all individuals within the population and its cellular tropism is limited to the intestinal cells [7,8], we cannot rule out there may be local changes in transcription in the intestinal cells or for certain individuals of CB4856. Transcriptional techniques, such as single-cell RNA-seq or TOMO-seq [48,49], that identify gene expression within infected cells could provide more details about the transcriptional response in the cells at stake.…”

Section: Transcriptional Activation Of the Ipr In Two Genetically DIVmentioning

confidence: 99%

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

Sluijs

Bosman

Pankok

et al. 2019

Preprint

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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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“…C. elegans possess only one population of stem cells-the germlinewhich originate from a single cell and become progressively more mature as they migrate through the gonad away from the distal tip cell (Kimble, 1981). In fact, previous studies have found mafr-1 enriched in the C. elegans germline, but the significance of this finding has never been studied (Ebbing et al, 2018;Grun et al, 2014;Han et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Roles for the RNA polymerase III regulator MAFR-1 in regulating sperm quality inCaenorhabditis elegans

Hammerquist

Curran

2020

Preprint

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The negative regulator of RNA polymerase (pol) III mafr-1 has been shown to affect RNA pol III transcript abundance, lipid biosynthesis and storage, progeny output, and lifespan. We deleted mafr-1 from the Caenorhabditis elegans genome and found that animals lacking mafr-1 replicated many phenotypes from previous RNAi-based studies, but strikingly not the oocyte-related reproductive phenotypes. Utilizing a yeast two-hybrid assay, we discovered several novel interactors of MAFR-1 that are expressed in a sperm-and germline-enriched manner. In support of a role for MAFR-1 in the male germline, we found mafr-1 null males have smaller spermatids that are less capable in competition for fertilization; a phenotype that was dependent on RNA pol III activity. Restoration of MAFR-1 expression specifically in the germline rescued the spermatid-related phenotypes, suggesting a cell autonomous role for MAFR-1 in nematode male fertility. Based on the high degree of conservation of Maf1 activity across species, our study may inform similar roles for Maf1 and RNA pol III in mammalian male fertility.

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Spatial Transcriptomics of C. elegans Males and Hermaphrodites Identifies Sex-Specific Differences in Gene Expression Patterns

Abstract: Highlights d 20 mm resolution AP gene expression maps of C. elegans males and hermaphrodites d Resource for in silico identification of cell-and tissuespecific genes d Identification of sex-specific germline and sperm genes

Cited by 70 publications

References 52 publications

Speciation and the developmental alarm clock

Speciation and the developmental alarm clock

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

Roles for the RNA polymerase III regulator MAFR-1 in regulating sperm quality inCaenorhabditis elegans

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