Temperature entrainment and DNA damage checkpoints in the Neurospora crassa circadian clock.

2004 ◽  
Author(s):  
António Manuel Magalhães. Pregueiro
Keyword(s):  
Dna Damage ◽  
Circadian Clock ◽  
Neurospora Crassa ◽  
Dna Damage Checkpoints ◽  
Temperature Entrainment

Overlapping Roles of the Spindle Assembly and DNA Damage Checkpoints in the Cell-Cycle Response to Altered Chromosomes in Saccharomyces cerevisiae

Genetics ◽  
2002 ◽  
Vol 161 (2) ◽  
pp. 521-534
Author(s):  
Peter M Garber ◽  
Jasper Rine
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Spindle Checkpoint ◽  
Dna Lesions ◽  
Replication Proteins ◽  
Replication Checkpoint ◽  
Dna Damage Checkpoints ◽  
Dna Replication Checkpoint ◽  
Mcm Proteins ◽  
Stalled Replication Forks

Abstract The MAD2-dependent spindle checkpoint blocks anaphase until all chromosomes have achieved successful bipolar attachment to the mitotic spindle. The DNA damage and DNA replication checkpoints block anaphase in response to DNA lesions that may include single-stranded DNA and stalled replication forks. Many of the same conditions that activate the DNA damage and DNA replication checkpoints also activated the spindle checkpoint. The mad2Δ mutation partially relieved the arrest responses of cells to mutations affecting the replication proteins Mcm3p and Pol1p. Thus a previously unrecognized aspect of spindle checkpoint function may be to protect cells from defects in DNA replication. Furthermore, in cells lacking either the DNA damage or the DNA replication checkpoints, the spindle checkpoint contributed to the arrest responses of cells to the DNA-damaging agent methyl methanesulfonate, the replication inhibitor hydroxyurea, and mutations affecting Mcm2p and Orc2p. Thus the spindle checkpoint was sensitive to a wider range of chromosomal perturbations than previously recognized. Finally, the DNA replication checkpoint did not contribute to the arrests of cells in response to mutations affecting ORC, Mcm proteins, or DNA polymerase δ. Thus the specificity of this checkpoint may be more limited than previously recognized.

scholarly journals COMPLEMENTATION ANALYSIS OF LINKED CIRCADIAN CLOCK MUTANTS OF NEUROSPORA CRASSA

Genetics ◽  
1976 ◽  
Vol 82 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Jerry F Feldman ◽  
Marian N Hoyle
Keyword(s):  
Linkage Group ◽  
Circadian Clock ◽  
Neurospora Crassa ◽  
Period Length ◽  
Complementation Analysis ◽  
Wild Type ◽  
The Right

ABSTRACT A fourth mutant of Neurospora crassa, designated frq-4, has been isolated in which the period length of the circadian conidiation rhythm is shortened to 19.3 ± 0.3 hours. This mutant is tightly linked to the three previously isolated frq mutants, and all four map to the right arm of linkage group VII about 10 map units from the centromere. Complementation tests suggest, but do not prove, that all four mutations are allelic, since each of the four mutants is co-dominant with the frq  + allele—i.e., heterokaryons have period lengths intermediate between the mutant and wild-type—and since heterokaryons between pairs of mutants also have period lengths intermediate between those of the two mutants.

scholarly journals Aberrant p53 alters DNA damage checkpoints in response to cisplatin: Downregulation of CDK expression and activity

2004 ◽  
Vol 112 (5) ◽  
pp. 760-770 ◽  
Author(s):  
Katharine H. Wrighton ◽  
Cecilia M. Prêle ◽  
Andrew Sunters ◽  
W. Andrew Yeudall
Keyword(s):  
Dna Damage ◽  
Dna Damage Checkpoints ◽  
Expression And Activity

scholarly journals Epistatic and Synergistic Interactions Between Circadian Clock Mutations in Neurospora crassa

Genetics ◽  
2001 ◽  
Vol 159 (2) ◽  
pp. 537-543
Author(s):  
Louis W Morgan ◽  
Jerry F Feldman
Keyword(s):  
Circadian Clock ◽  
Neurospora Crassa ◽  
Mutant Strain ◽  
Temperature Compensation ◽  
Double Mutant ◽  
Synergistic Interactions ◽  
Long Period ◽  
Double Mutant Strain ◽  
Short Period ◽  
Compensation Mechanisms

Abstract We identified a series of epistatic and synergistic interactions among the circadian clock mutations of Neurospora crassa that indicate possible physical interactions among the various clock components encoded by these genes. The period-6 (prd-6) mutation, a short-period temperature-sensitive clock mutation, is epistatic to both the prd-2 and prd-3 mutations. The prd-2 and prd-3 long-period mutations show a synergistic interaction in that the period length of the double mutant strain is considerably longer than predicted. In addition, the prd-2 prd-3 double mutant strain also exhibits overcompensation to changes in ambient temperature, suggesting a role in the temperature compensation machinery of the clock. The prd-2, prd-3, and prd-6 mutations also show significant interactions with the frq7 long-period mutation. These results suggest that the gene products of prd-2, prd-3, and prd-6 play an important role in both the timing and temperature compensation mechanisms of the circadian clock and may interact with the FRQ protein.

Synchronizing the Neurospora crassa circadian clock with the rhythmic environment

2005 ◽  
Vol 33 (5) ◽  
pp. 949-952 ◽  
Author(s):  
N. Price-Lloyd ◽  
M. Elvin ◽  
C. Heintzen
Keyword(s):  
Light Intensity ◽  
Circadian Clock ◽  
Neurospora Crassa ◽  
Model Organism ◽  
Circadian Clocks ◽  
Current Understanding ◽  
Signalling Pathways ◽  
Selection Pressures ◽  
The Earth ◽  
Natural Cycles

The metronomic predictability of the environment has elicited strong selection pressures for the evolution of endogenous circadian clocks. Circadian clocks drive molecular and behavioural rhythms that approximate the 24 h periodicity of our environment. Found almost ubiquitously among phyla, circadian clocks allow preadaptation to rhythms concomitant with the natural cycles of the Earth. Cycles in light intensity and temperature for example act as important cues that couple circadian clocks to the environment via a process called entrainment. This review summarizes our current understanding of the general and molecular principles of entrainment in the model organism Neurospora crassa, a simple eukaryote that has one of the best-studied circadian systems and light-signalling pathways.

4 From Genetics to Molecular Oscillations: The Circadian Clock in Neurospora crassa

2020 ◽  
pp. 77-103
Author(s):  
Meaghan S. Jankowski ◽  
Zachary A. Chase ◽  
Jennifer M. Hurley
Keyword(s):  
Circadian Clock ◽  
Neurospora Crassa

scholarly journals DNA damage shifts circadian clock time via Hausp-dependent Cry1 stabilization

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Stephanie J Papp ◽  
Anne-Laure Huber ◽  
Sabine D Jordan ◽  
Anna Kriebs ◽  
Madelena Nguyen ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Circadian Clock ◽  
Transcriptional Response ◽  
Genotoxic Stress ◽  
Genomic Integrity ◽  
Clock Time ◽  
Dna Repair Enzymes ◽  
Repair Enzymes ◽  
Specific Protease

The circadian transcriptional repressors cryptochrome 1 (Cry1) and 2 (Cry2) evolved from photolyases, bacterial light-activated DNA repair enzymes. In this study, we report that while they have lost DNA repair activity, Cry1/2 adapted to protect genomic integrity by responding to DNA damage through posttranslational modification and coordinating the downstream transcriptional response. We demonstrate that genotoxic stress stimulates Cry1 phosphorylation and its deubiquitination by Herpes virus associated ubiquitin-specific protease (Hausp, a.k.a Usp7), stabilizing Cry1 and shifting circadian clock time. DNA damage also increases Cry2 interaction with Fbxl3, destabilizing Cry2. Thus, genotoxic stress increases the Cry1/Cry2 ratio, suggesting distinct functions for Cry1 and Cry2 following DNA damage. Indeed, the transcriptional response to genotoxic stress is enhanced in Cry1−/− and blunted in Cry2−/− cells. Furthermore, Cry2−/− cells accumulate damaged DNA. These results suggest that Cry1 and Cry2, which evolved from DNA repair enzymes, protect genomic integrity via coordinated transcriptional regulation.

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