Analysis of the light regulatory mechanism in carotenoid production in Rhodosporidium toruloides NBRC 10032

2021 ◽  
Author(s):  
Khanh Dung Pham ◽  
Yuuki Hakozaki ◽  
Takeru Takamizawa ◽  
Atsushi Yamazaki ◽  
Harutake Yamazaki ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Oleaginous Yeast ◽  
Gene Activation ◽  
Light Response ◽  
Carotenoid Biosynthesis ◽  
Rhodosporidium Toruloides ◽  
End Joining ◽  
Carotenoid Production ◽  
Non Homologous End Joining

Abstract Light stimulates carotenoid production in an oleaginous yeast Rhodosporidium toruloides NBRC 10032 by promoting carotenoid biosynthesis genes. These genes undergo two-step of transcriptional activation. The potential light regulator, Cryptochrome DASH (CRY1), has been suggested to contribute to this mechanism. In this study, based on KU70 (a component of non-homologous end joining (NHEJ)) disrupting background, CRY1 disruptant was constructed to clarify CRY1 function. From analysis of CRY1 disruptant, it was suggested that CRY1 has the activation role of the carotenogenic gene expression. To obtain further insights into the light response, mutants varying carotenoid production were generated. Through analysis of mutants, the existence of the control two-step gene activation was proposed. In addition, our data analysis showed the strong possibility that R. toruloides NBRC 10032 is a homo-diploid strain.

scholarly journals The role of RecQ helicases in non-homologous end-joining

2014 ◽  
Vol 49 (6) ◽  
pp. 463-472 ◽  
Author(s):  
Guido Keijzers ◽  
Scott Maynard ◽  
Raghavendra A. Shamanna ◽  
Lene Juel Rasmussen ◽  
Deborah L. Croteau ◽  
...  
Keyword(s):  
End Joining ◽  
Recq Helicases ◽  
Non Homologous End Joining

The role of the non-homologous end-joining pathway in lymphocyte development

2004 ◽  
Vol 200 (1) ◽  
pp. 115-131 ◽  
Author(s):  
Sean Rooney ◽  
Jayanta Chaudhuri ◽  
Frederick W. Alt
Keyword(s):  
Lymphocyte Development ◽  
End Joining ◽  
Non Homologous End Joining

scholarly journals Evidence for a Bigenic Chromatin Subdomain in Regulation of the Fetal-to-Adult Hemoglobin Switch

2008 ◽  
Vol 29 (6) ◽  
pp. 1635-1648 ◽  
Author(s):  
Hugues Beauchemin ◽  
Marie Trudel
Keyword(s):  
Transcriptional Activation ◽  
Gene Activation ◽  
Dna Demethylation ◽  
Open Chromatin ◽  
Chromosome Conformation ◽  
Hemoglobin Switching ◽  
Switching Patterns ◽  
Adult Hemoglobin ◽  
Globin Promoter

ABSTRACT During development, human β-globin locus regulation undergoes two critical switches, the embryonic-to-fetal and fetal-to-adult hemoglobin switches. To define the role of the fetal Aγ-globin promoter in switching, human β-globin-YAC transgenic mice were produced with the Aγ-globin promoter replaced by the erythroid porphobilinogen deaminase (PBGD) promoter (PBGDAγ-YAC). Activation of the stage-independent PBGDAγ-globin strikingly stimulated native Gγ-globin expression at the fetal and adult stages, identifying a fetal gene pair or bigenic cooperative mechanism. This impaired fetal silencing severely suppressed both δ- and β-globin expression in PBGDAγ-YAC mice from fetal to neonatal stages and altered kinetics and delayed switching of adult β-globin. This regulation evokes the two human globin switching patterns in the mouse. Both patterns of DNA demethylation and chromatin immunoprecipitation analysis correlated with gene activation and open chromatin. Locus control region (LCR) interactions detected by chromosome conformation capture revealed distinct spatial fetal and adult LCR bigenic subdomains. Since both intact fetal promoters are critical regulators of fetal silencing at the adult stage, we concluded that fetal genes are controlled as a bigenic subdomain rather than a gene-autonomous mechanism. Our study also provides evidence for LCR complex interaction with spatial fetal or adult bigenic functional subdomains as a niche for transcriptional activation and hemoglobin switching.

scholarly journals Loss of Cdc13 causes genome instability by a deficiency in replication-dependent telomere capping

2019 ◽  
Author(s):  
Rachel E Langston ◽  
Dominic Palazzola ◽  
Erin Bonnell ◽  
Raymund J. Wellinger ◽  
Ted Weinert
Keyword(s):  
Homologous Recombination ◽  
Genome Stability ◽  
Genome Instability ◽  
Chromosome Instability ◽  
S Phase ◽  
Temperature Sensitive ◽  
End Joining ◽  
Telomere Capping ◽  
Non Homologous End Joining

AbstractIn budding yeast, Cdc13, Stn1, and Ten1 form a telomere binding heterotrimer dubbed CST. Here we investigate the role of Cdc13/CST in maintaining genome stability, using a Chr VII disome system that can generate recombinants, loss, and enigmatic unstable chromosomes. In cells expressing a temperature sensitive CDC13 allele, cdc13F684S, unstable chromosomes frequently arise due to problems in or near a telomere. Hence, when Cdc13 is defective, passage through S phase causes Exo1-dependent ssDNA and unstable chromosomes, which then are the source for whole chromosome instability events (e.g. recombinants, chromosome truncations, dicentrics, and/or loss). Specifically, genome instability arises from a defect in Cdc13’s replication-dependent telomere capping function, not Cdc13s putative post-replication telomere capping function. Furthermore, the unstable chromosomes form without involvement of homologous recombination nor non-homologous end joining. Our data suggest that a Cdc13/CST defect in semi-conservative replication near the telomere leads to ssDNA and unstable chromosomes, which then are lost or subject to complex rearrangements. This system defines a links between replication-dependent chromosome capping and genome stability in the form of unstable chromosomes.

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