Effect of the diet type and temperature on the<i>C. elegans</i>transcriptome

Gómez-Orte, Eva; Cornes, Eric; Zheleva, Angelina; Sáenz-Narciso, Beatriz; Toro, María de; Íñiguez, María; López, Rosa; San-Juan, Juan F.; Ezcurra, Begoña; Sacristan, B.; Sánchez-Blanco, Adolfo; Cerón, Julián; Cabello, Juan

doi:10.18632/oncotarget.23563

Cited by 38 publications

(47 citation statements)

References 54 publications

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“…The FAT-5 desaturase is specific for the synthesis of palmitic acid (16:0), whereas the FAT-6 and FAT-7 desaturases, which share 86% homology at the nucleotide level, mainly desaturate stearic acid (18:0), producing a C18:1 MUFA called oleic acid (C18:1(9z), OA) (Brock et al 2006b;Watts and Browse, 2000) . Consistent with previous reports (Murray et al 2007;Savory et al, 2011b;Gómez-Orte et al, 2018), we observe that there is a 38-40% decrease in transcript levels of fat-6 and fat-7 as the temperature increases from 15℃ to 20℃. The levels of fat-6 do not decrease further at 25℃ (Figure S1C), though fat-7 declines to 6% of its levels at 15℃ (Figure S1B, Supp.…”

Section: Introductionsupporting

confidence: 93%

A neuronal thermostat controls membrane fluidity inC. elegans

Casanueva

Chauve

Murdoch

et al. 2019

Preprint

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An organisms' ability to adapt to heat can be key to its survival. Cells adapt to temperature shifts by adjusting lipid desaturation levels and the fluidity of membranes in a process that is thought to be controlled cell autonomously. We have discovered that subtle, step-wise increments in ambient temperature can lead to the conserved heat shock response being activated in head neurons of C. elegans. This response is exactly opposite to the expression of the lipid desaturase FAT-7 in the worm's gut. We find that the over-expression of the master regulator of this response, Hsf-1, in head neurons, causes extensive fat remodeling to occur across tissues. These changes include a decrease in FAT-7 expression and a shift in the levels of unsaturated fatty acids in the plasma membrane. These shifts are in line with membrane fluidity requirements to survive in warmer temperatures. We have identified that the cGMP receptor, TAX-2/TAX-4, as well as TGF-β/BMP signaling, as key players in the transmission of neuronal stress to peripheral tissues. This is the first study to suggest that a thermostat-based mechanism can centrally coordinate membrane fluidity in response to warm temperatures across tissues in multicellular animals. 2004; Hedgecock and Russell, 1975)Although thermostat-based behaviours help ectotherms to escape noxious stimuli like heat, the longer-term survival of ectotherms when environmental temperatures change depends on their ability to remodel lipids within the plasma membrane, which is highly sensitive to external temperatures. Homeoviscous adaptation (HVA) is a mechanism that regulates the viscosity and permeability of membranes to ensure the robustness of biochemical reactions (Sinensky 1974;Cossins and Prosser 1978). In homeoviscous cold adaptation, membrane bilayers undergo a reversible change of state from a non-fluid (ordered) to a fluid (disordered) structure whereby the membrane's phospholipids (PLs) fatty acyl (FA) chains become increasingly unsaturated (Mendoza 2014; Ernst, Ejsing, and Antonny 2016). In C. elegans, three Δ9-acyl desaturase both the regulators of SCD enzymes -such as MDT-15-and SCD enzymes themselves are known to negatively regulate HSP expression at 15°C 19 (Savory et al 2011a) . However, it is not known whether Hsf-1 dependent cellular responses can modulate SCD expression and MUFA levels.Here, we show that hsp transcripts are expressed primarily in the head neurons of C. elegans at 20°C and show a clear temperature-sensitive expression pattern. We used the neuronal overexpression of HSF-1 (nhsf-1) as a tool to study the consequences of ectopically activating HSR in neurons at 20°C. We find that HSF-1 overexpression, via nhsf-1, in addition to its previously described role in controlling peripheral stress responses and longevity (Douglas et al. 2015), remodels lipid metabolism. This function is performed by decreasing the expression of fat-7 in the intestine, whilst activating the expression of catabolic lysosomal lipases. We identified the cGMP receptors TAX-2/TAX-4 and TGF-β...

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Section: Introductionsupporting

confidence: 93%

A neuronal thermostat controls membrane fluidity inC. elegans

Casanueva

Chauve

Murdoch

et al. 2019

Preprint

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“…The Cer19 genes and also many ERGO-1-ERI-6/7 targets are expressed exclusively at higher temperatures (at 25°C): of the 183 genes identified that only are expressed at 25°C and not at 15°C or 20°C (33), 33 genes are ERGO-1-ERI-6/7 targets (Supplemental Figure 5E). This increase in expression at 25°C is accompanied by a reduced expression of critical silencing factors eri-6/7 , emb-4 and drh-3 (33). Cer19 retrotransposons are also expressed in response to heat shock (34).…”

Section: Hsf-1/hsf1 Regulates Upr Genes and Retrotransposonsmentioning

confidence: 99%

Caenorhabditis elegans ADAR editing and the ERI-6/7/MOV10 RNAi pathway silence endogenous viral elements and LTR retrotransposons

Fischer

Ruvkun

2019

Preprint

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18Endogenous retroviruses and LTR retrotransposons are mobile genetic elements that 19 are closely related to retroviruses. Desilenced endogenous retroviruses are associated 20 with human autoimmune disorders and neurodegenerative diseases. C. elegans and 21 related Caenorhabdites contain LTR retrotransposons and, as described here, 22 numerous integrated viral genes including viral envelope genes that are part of LTR 23 retrotransposons. We found that both LTR retrotransposons and endogenous viral 24 elements are silenced by ADARs (adenosine deaminases acting on double-stranded 25 RNA (dsRNA)) together with the endogenous RNAi factor ERI-6/7, a homolog of Mov10 26 helicase, a retrotransposon and retrovirus restriction factor in human. siRNAs 27 Transposons can have profound effects on cellular function such as disruption of gene 53 function by transposon insertion, cell death as a consequence of transposon-induced 54 double stranded breaks, and genomic rearrangements caused by homologous 55 recombination between repeat elements. Retrotransposons and endogenous 56 retroviruses may affect cellular function through overexpression of toxic proteins or the 57 activity of retroviral proteins on endogenous sequences. Palindromic repeat elements 58 such as those formed by adjacent but inverted insertion of vertebrate Alu elements 59 into genes can cause the accumulation of dsRNA. 60 Many RNA viruses replicate via a dsRNA intermediate, which is detected to 61 trigger an interferon-based antiviral response in mammals and an RNA interference 62 response in invertebrates. To avoid an anti-viral response to endogenous palindromic 63 dsRNAs when in fact there is no viral infection, ADARs edit adenosines to inosines in 64 endogenous dsRNA destabilizing the RNA duplex and thus preventing recognition by 65

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“…This raises the possibility that mab-5 levels may relate to the enhanced sensitivity of V6a cells with respect to undergoing a cell fate change. Higher temperatures are thought to generally increase levels of gene expression, but this relationship varies from one gene to another (Gomez-Orte et al . 2018).…”

Section: Discussionmentioning

confidence: 99%

A cell fate switch in theC. elegansseam cell lineage occurs through modulation of the Wnt asymmetry pathway in response to temperature increase

Barkoulas

Hintze²,

Koneru³

et al. 2019

Preprint

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23Populations often display consistent developmental phenotypes across individuals 24 despite the inevitable biological stochasticity. Nevertheless, developmental robustness 25 has limits and systems can fail upon change in the environment or the genetic 26 background. We use here the seam cells, a population of epidermal stem cells in 27 Caenorhabditis elegans, to study the influence of temperature change and genetic 28 variation on cell fate. Seam cell development has mostly been studied so far in the lab 29 reference strain (N2), grown at 20° temperature. We demonstrate that an increase in 30 culture temperature to 25°, introduces variability in the wild-type seam cell lineage with a 31 proportion of animals showing an increase in seam cell number. We map this increase to 32 lineage-specific symmetrisation events of normally asymmetric cell divisions at the final 33 larval stage, leading to the retention of seam cell fate in both daughter cells. Using 34 genetics and single molecule imaging, we demonstrate that this symmetrisation occurs 35 via changes in the Wnt asymmetry pathway, leading to aberrant Wnt target activation in 36 anterior cell daughters. We find that intrinsic differences in the Wnt asymmetry pathway 37 already exist between seam cells at 20° and this may sensitise cells towards a cell fate 38 switch at increased temperature. Finally, we demonstrate that wild isolates of C. elegans 39 display variation in seam cell sensitivity to increased culture temperature, although seam 40 cell numbers are comparable when raised at 20°. Our results highlight how temperature 41 can modulate cell fate decisions in an invertebrate model of stem cell patterning. 42 43 44 45 46 47 48 During development, organisms must withstand environmental and genetic perturbations 49 to produce consistent phenotypes (Felix and Barkoulas 2012). These phenotypes are 50 often a product of complex developmental events that require a tight balance between cell 51 division and cell differentiation (Soufi and Dalton 2016). A key example is stem cell 52 divisions, consisting of highly controlled asymmetric and symmetric patterns, which are 53 vital for generating cell diversity, as well as maintaining cell numbers in tissues and organs 54 (Morrison and Kimble 2006; Knoblich 2008). Developmental robustness has inherent 55 limits and certain perturbations can push a system outside its buffering zone (Braendle 56 and Felix 2008; Barkoulas et al. 2013). In these cases, it is also important to understand 57 how systems fail by investigating how perturbations precisely modulate developmental 58 processes. Here we address the question of how changes in environmental temperature 59 can affect cell fate outcomes using the nematode C. elegans as a model system. While it 60 is well known that increasing or decreasing environmental temperature can change the 61 development speed in C. elegans, the effect of temperature on specific cell division and 62 fate acquisition events is less well understood. The C. elegans adult hermaphrodite 63 co...

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Effect of the diet type and temperature on theC. eleganstranscriptome

Cited by 38 publications

References 54 publications

A neuronal thermostat controls membrane fluidity inC. elegans

A neuronal thermostat controls membrane fluidity inC. elegans

Caenorhabditis elegans ADAR editing and the ERI-6/7/MOV10 RNAi pathway silence endogenous viral elements and LTR retrotransposons

A cell fate switch in theC. elegansseam cell lineage occurs through modulation of the Wnt asymmetry pathway in response to temperature increase

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