Circadian Rhythms in
            <i>Neurospora crassa</i>
            and Other Filamentous Fungi

Liu, Yi; Bell-Pedersen, Deborah

doi:10.1128/ec.00133-06

Cited by 131 publications

(121 citation statements)

References 117 publications

(231 reference statements)

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“…Neurospora crassa, a model organism for the study of circadian rhythms (Lakin-Thomas et al 1990;Dunlap and Loros 2006;Liu and Bell-Pedersen 2006), expresses its rhythm by alternating areas of asexual spore formation (conidiation) with areas of thinner hyphal growth without spore formation when growing on solid agar medium. Areas of spore formation are known as ''bands'' and thinner areas without spore formation are known as ''interbands.''…”

Section: Ircadian Rhythms Are Biological Rhythms Withmentioning

confidence: 99%

“…There are also positive feedback mechanisms involving the influence of frq expression on wc-1 and wc-2 activity and an important role played by post-translational modifications and protein degradation. Details may be found in recent reviews (Lakin-Thomas and Brody 2004;Liu 2005;Brunner and Schafmeier 2006;Dunlap 2006;Liu and Bell-Pedersen 2006).…”

Section: Ircadian Rhythms Are Biological Rhythms Withmentioning

confidence: 99%

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Rhythmic Conidiation in Constant Light inVividMutants ofNeurospora crassa

et al. 2009

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Section: Ircadian Rhythms Are Biological Rhythms Withmentioning

confidence: 99%

Section: Ircadian Rhythms Are Biological Rhythms Withmentioning

confidence: 99%

Rhythmic Conidiation in Constant Light inVividMutants ofNeurospora crassa

et al. 2009

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“…The eukaryotic circadian clock oscillator contains positive and negative elements that form auto-regulatory negative feedback loops (2)(3)(4)(5)(6)(7)(8).…”

mentioning

confidence: 99%

Suppression of WHITE COLLAR-independent frequency Transcription by Histone H3 Lysine 36 Methyltransferase SET-2 Is Necessary for Clock Function in Neurospora

Sun

Zhou

Xiao

et al. 2016

Journal of Biological Chemistry

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The circadian system in Neurospora is based on the transcriptional/translational feedback loops and rhythmic frequency (frq) transcription requires the WHITE COLLAR (WC) complex. Our previous paper has shown that frq could be transcribed in a WC-independent pathway in a strain lacking the histone H3K36 methyltransferase, SET-2 (su(var)3-9-enhancer-of-zestetrithorax-2) (1), but the mechanism was unclear. Here we disclose that loss of histone H3K36 methylation, due to either deletion of SET-2 or H3K36R mutation, results in arrhythmic frq transcription and loss of overt rhythmicity. Histone acetylation at frq locus increases in set-2 KO mutant. Consistent with these results, loss of H3K36 methylation readers, histone deacetylase RPD-3 (reduced potassium dependence 3) or EAF-3 (essential SAS-related acetyltransferase-associated factor 3), also leads to hyperacetylation of histone at frq locus and WC-independent frq expression, suggesting that proper chromatin modification at frq locus is required for circadian clock operation. Furthermore, a mutant strain with three amino acid substitutions (histone H3 lysine 9, 14, and 18 to glutamine) was generated to mimic the strain with hyperacetylation state of histone H3. H3K9QK14QK18Q mutant exhibits the same defective clock phenotype as rpd-3 KO mutant. Our results support a scenario in which H3K36 methylation is required to establish a permissive chromatin state for circadian frq transcription by maintaining proper acetylation status at frq locus.Despite evolutionary distance, circadian clock oscillators are conserved among the organisms to perform their cellular and behavioral activities. The eukaryotic circadian clock oscillator contains positive and negative elements that form auto-regulatory negative feedback loops (2-8).In the Neurospora circadian negative feedback loop, the GATA-family transcription factors WHITE COLLAR-1 (WC-1) 3 and WHITE COLLAR-2 (WC-2) serve as positive elements. Typically, WC-1 and WC-2 form a heterodimer through their Per-Arnt-Sim (PAS) domain and rhythmically bind the promoter of the clock gene frequency (frq) to activate its transcription. FREQUENCY (FRQ) and its partner FRQ-interacting RNA helicase (FRH) act as negative elements. FRQ is the core factor in Neurospora oscillator, which determines the normal clock rhythm (9 -16). The translated FRQ interacts with FRH and forms the FFC (FRQ-FRH complex) to inhibit its own transcription by suppressing the activity of the WC complex. FRQ is progressively phosphorylated and degraded through the ubiquitin-proteasome pathway. Degradation of FRQ derepresses the WC complex, initiating a new circle of frq transcription (14,(17)(18)(19). The circadian oscillator creates a robust rhythmic system with a period of ϳ22 h in Neurospora crassa (17,20). Rhythmic activation and repression of frq transcription result in cyclic changes of frq mRNA abundance. In Neurospora, histone modifiers and chromatin remodelers are required for rhythmic transcription of frq gene and clock-controlled genes (1, 9, 22-24). Howeve...

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“…Thus, cells have evolved mechanisms to adapt to prolonged light exposure while retaining sensitivity to escalating changes in light intensity at the same time. Light responses in the filamentous fungus Neurospora crassa have been studied for several decades because of their robustness and easily scored phenotypes (1)(2)(3)(4)(5)(6). The WHITE COLLAR (WC)-1 and WC-2 proteins control most light responses in Neurospora (7,8).…”

mentioning

confidence: 99%

Physical interaction between VIVID and white collar complex regulates photoadaptation inNeurospora

Chen¹,

DeMay

Gladfelter

et al. 2010

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

137

166

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Photoadaptation, the ability to attenuate a light response on prolonged light exposure while remaining sensitive to escalating changes in light intensity, is essential for organisms to decipher time information appropriately, yet the underlying molecular mechanisms are poorly understood. In Neurospora crassa, VIVID (VVD), a small LOV domain containing blue-light photoreceptor protein, affects photoadaptation for most if not all light-responsive genes. We report that there is a physical interaction between VVD and the white collar complex (WCC), the primary blue-light photoreceptor and the transcription factor complex that initiates light-regulated transcriptional responses in Neurospora. Using two previously characterized VVD mutants, we show that the level of interaction is correlated with the level of WCC repression in constant light and that even lightinsensitive VVD is sufficient partly to regulate photoadaptation in vivo. We provide evidence that a functional GFP-VVD fusion protein accumulates in the nucleus on light induction but that nuclear localization of VVD does not require light. Constitutively expressed VVD alone is sufficient to change the dynamics of photoadaptation. Thus, our results demonstrate a direct molecular connection between two of the most essential light signaling components in Neurospora, VVD and WCC, illuminating a previously uncharacterized process for light-sensitive eukaryotic cells.light | white collar-1 | white collar-2 | photoreceptor | LOV domain

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Circadian Rhythms in Neurospora crassa and Other Filamentous Fungi

Cited by 131 publications

References 117 publications

Rhythmic Conidiation in Constant Light inVividMutants ofNeurospora crassa

Rhythmic Conidiation in Constant Light inVividMutants ofNeurospora crassa

Suppression of WHITE COLLAR-independent frequency Transcription by Histone H3 Lysine 36 Methyltransferase SET-2 Is Necessary for Clock Function in Neurospora

Physical interaction between VIVID and white collar complex regulates photoadaptation inNeurospora

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