Circadian period lengths of lipid synthesis mutants (cel,chol-1) ofNeurosporashow defective temperature, but intact pH-compensation

Ruoff, Peter; Slewa, Ieda

doi:10.1081/cbi-120004222

Cited by 8 publications

(4 citation statements)

References 31 publications

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“…We confirmed that strain PL32-54 (bd;chol-1;csp-1) displays a characteristic elongated rhythm (period length Ϸ 60 h) on race tubes without choline supplementation and a normal conidiation rhythm (period length Ϸ 22 h) on race tubes supplemented with 100 M choline (Fig. 1A), consistent with previous results (30,32). To measure molecular rhythms in liquid cultures, bd;chol-1;csp-1 was cultured with or without choline supplementation for 12-56 h in light followed, respectively, by 48 to 4 h in darkness, so by harvest all cultures had been growing with or without choline supplementation for at least 60 h (34).…”

Section: Frq Oscillation In Choline Depletionsupporting

confidence: 81%

“…The mutant shows a conidiation rhythm, controlled by a choline deficiency oscillator (CDO), with a period Ͼ50 h under choline starvation (30) that can be entrained by light to periods near its intrinsic length but not to periods within the circadian range. The rhythm is pH-compensated but not temperature-compensated (30)(31)(32). The period length of the rhythm reflects the degree of choline starvation, but the allelic states of the frq or wc genes have little or no effect on the rhythm.…”

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confidence: 99%

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A developmental cycle masks output from the circadian oscillator under conditions of choline deficiency in Neurospora

Shi

Larrondo²,

Loros³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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In Neurospora, metabolic oscillators coexist with the circadian transcriptional/translational feedback loop governed by the FRQ (Frequency) and WC (White Collar) proteins. One of these, a choline deficiency oscillator (CDO) observed in chol-1 mutants grown under choline starvation, drives an uncompensated long-period developmental cycle (Ϸ60 -120 h). To assess possible contributions of this metabolic oscillator to the circadian system, molecular and physiological rhythms were followed in liquid culture under choline starvation, but these only confirmed that an oscillator with a normal circadian period length can run under choline starvation. This finding suggested that long-period developmental cycles elicited by nutritional stress could be masking output from the circadian system, although a caveat was that the CDO sometimes requires several days to become consolidated. To circumvent this and observe both oscillators simultaneously, we used an assay using a codon-optimized luciferase to follow the circadian oscillator. Under conditions where the long-period, uncompensated, CDO-driven developmental rhythm was expressed for weeks in growth tubes, the luciferase rhythm in the same cultures continued in a typical compensated manner with a circadian period length dependent on the allelic state of frq. Periodograms revealed no influence of the CDO on the circadian oscillator. Instead, the CDO appears as a cryptic metabolic oscillator that can, under appropriate conditions, assume control of growth and development, thereby masking output from the circadian system. frqdriven luciferase as a reporter of the circadian oscillator may in this way provide a means for assessing prospective role(s) of metabolic and/or ancillary oscillators within cellular circadian systems.Frequency-less oscillator ͉ clock

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Section: Frq Oscillation In Choline Depletionsupporting

confidence: 81%

mentioning

confidence: 99%

A developmental cycle masks output from the circadian oscillator under conditions of choline deficiency in Neurospora

Shi

Larrondo²,

Loros³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…Fatty acid synthesis mutants of Neurospora crassa have a long‐period circadian phenotype and/or defective temperature compensation (Lakin‐Thomas & Brody, 2000; Ruoff & Slewa, 2002). In Arabidopsis , mutation of FAD2 means that the free‐running period of leaf movement does not shorten as it does in wild‐type plants when grown at 27°C (Fig.…”

Section: Discussionmentioning

confidence: 99%

Homeostasis of plasma membrane viscosity in fluctuating temperatures

et al. 2011

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Summary• Temperature has a direct effect at the cellular level on an organism. For instance, in the case of biomembranes, cooling causes lipids to lose entropy and pack closely together. Reducing temperature should, in the absence of other factors, increase the viscosity of a lipid membrane. We have investigated the effect of temperature variation on plasma membrane (PM) viscosity.• We used dispersion tracking of photoactivated green fluorescent protein (GFP) and fluorescence recovery after photobleaching in wild-type and desaturase mutant Arabidopsis thaliana plants along with membrane lipid saturation analysis to monitor the effect of temperature and membrane lipid composition on PM viscosity.• Plasma membrane viscosity in A. thaliana is negatively correlated with ambient temperature only under constant-temperature conditions. In the more natural environment of temperature cycles, plants actively manage PM viscosity to counteract the direct effects of temperature.• Plasma membrane viscosity is regulated by altering the proportion of desaturated fatty acids. In cold conditions, cell membranes accumulate desaturated fatty acids, which decreases membrane viscosity and vice versa. Moreover, we show that control of fatty acid desaturase 2 (FAD2)-dependent lipid desaturation is essential for this homeostasis of membrane viscosity. Finally, a lack of FAD2 function results in aberrant temperature responses.

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“…The conidiation phenotypes of the multiplemutant strains were assayed in free-running conditions (DD, 22 °C) on medium without choline. Choline-free medium reduces the growth rate of chol-1 strains and allows expression of long-period rhythmicity in both frq + and frq null strains (Lakin-Thomas, 1996, 1998Lakin-Thomas and Brody, 2000;Ruoff and Slewa, 2002;Shi et al, 2007). In Figure 1, the "wildtype" strain (carrying the ras-1 bd and csp-1 mutations but wild type for chol-1, frq, and prd) displays the expected conidiation rhythmicity.…”

Section: Effects Of Prd Mutations On Free-running Rhythms In Chol-1mentioning

confidence: 99%

Effects ofprdCircadian Clock Mutations on FRQ-Less Rhythms inNeurospora

Lakin-Thomas

2010

J Biol Rhythms

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Rhythmic conidiation (spore formation) in Neurospora crassa provides a model system for investigating the molecular mechanisms of circadian rhythmicity. A feedback loop involving the frq, wc-1, and wc-2 gene products (FRQ/ WCC) is an important component of the mechanism; however, rhythmic conidiation can still be observed when these gene products are absent. The nature of the oscillator(s) that drives this FRQ-less rhythmicity (FLO) is an important question in Neurospora circadian biology. We have looked for interactions between FRQ/WCC and FLO by assaying the effects on FRQ-less rhythms of mutations known to affect the period in the presence of FRQ. We assayed 4 prd mutations (prd-1, prd-2, prd-3, and prd-4) under 2 conditions in frq(null) strains: long-period free-running rhythms in chol-1 strains grown without choline, and heat-entrainable rhythms in choline-sufficient conditions. We found effects of all 4 mutations on both types of FRQ-less rhythms. The greatest effects were seen with prd-1 and prd-2, which abolished free-running rhythms in the chol-1; frq(10) backgrounds and significantly affected entrained peak timing under heat-entrainment conditions in frq( 10) backgrounds. The prd-3 and prd-4 mutations had more subtle effects on period and stability of free-running rhythms in the chol-1; frq(10) backgrounds and had little effect on peak timing under heat-entrainment conditions in frq(10) backgrounds. These results, along with previously published evidence for effects of prd mutations on other FRQ-less rhythms, suggest that either there are common components shared between the FRQ/WCC oscillator and several FRQ-less oscillators or that there is a single oscillator driving all conidiation rhythms. We favor a model of the Neurospora circadian system in which a single FRQ-less oscillator drives conidiation and interacts with the FRQ/WCC feedback loop; the output or amplitude of the FRQ-less oscillator can be affected by many gene products and metabolic conditions that reveal FRQ-less rhythmicity. We propose that prd-1 and prd-2 are good candidates for components of the FRQ-less oscillator and that prd-3 and prd-4 act on the system mainly through effects on FRQ/WCC.

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Circadian period lengths of lipid synthesis mutants (cel,chol-1) ofNeurosporashow defective temperature, but intact pH-compensation

Cited by 8 publications

References 31 publications

A developmental cycle masks output from the circadian oscillator under conditions of choline deficiency in Neurospora

A developmental cycle masks output from the circadian oscillator under conditions of choline deficiency in Neurospora

Homeostasis of plasma membrane viscosity in fluctuating temperatures

Effects ofprdCircadian Clock Mutations on FRQ-Less Rhythms inNeurospora

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