scholarly journals Towards a synthetic nuclear transcription system in green algae: Characterization of Chlamydomonas reinhardtii nuclear transcription factors and identification of targeted promoters

2017 ◽  
Vol 22 ◽  
pp. 47-55 ◽  
Author(s):  
Melissa S. Anderson ◽  
Travis J. Muff ◽  
David R. Georgianna ◽  
Stephen P. Mayfield
1997 ◽  
Vol 151 (3) ◽  
pp. 262-268 ◽  
Author(s):  
Junko Kato ◽  
Toshiaki Yamahara ◽  
Katsuyuki Tanaka ◽  
Susumu Takio ◽  
Toshio Satoh

Author(s):  
Araceli García-Martínez ◽  
Sandra Silva-Ortega ◽  
Beatriz López-Muñoz ◽  
Óscar Moreno-Pérez ◽  
Irene Monjas ◽  
...  

2009 ◽  
Vol 33 (5) ◽  
pp. 860-865
Author(s):  
Lan-Lan LU ◽  
Gen-Bao LI ◽  
Yin-Wu SHEN ◽  
Ming-Ming HU ◽  
Yong-Ding LIU

Genetics ◽  
2001 ◽  
Vol 158 (3) ◽  
pp. 1051-1060
Author(s):  
Claire Remacle ◽  
Denis Baurain ◽  
Pierre Cardol ◽  
René F Matagne

Abstract The mitochondrial rotenone-sensitive NADH:ubiquinone oxidoreductase (complex I) comprises more than 30 subunits, the majority of which are encoded by the nucleus. In Chlamydomonas reinhardtii, only five components of complex I are coded for by mitochondrial genes. Three mutants deprived of complex I activity and displaying slow growth in the dark were isolated after mutagenic treatment with acriflavine. A genetical analysis demonstrated that two mutations (dum20 and dum25) affect the mitochondrial genome whereas the third mutation (dn26) is of nuclear origin. Recombinational analyses showed that dum20 and dum25 are closely linked on the genetic map of the mitochondrial genome and could affect the nd1 gene. A sequencing analysis confirmed this conclusion: dum20 is a deletion of one T at codon 243 of nd1; dum25 corresponds to a 6-bp deletion that eliminates two amino acids located in a very conserved hydrophilic segment of the protein.


Genetics ◽  
1997 ◽  
Vol 146 (4) ◽  
pp. 1345-1363 ◽  
Author(s):  
Hélène George ◽  
Régine Terracol

We report here the genetical and molecular characterization of a new Drosophila zygotic lethal locus, vrille (vri). vri alleles act not only as dominant maternal enhancers of embryonic dorsoventral patterning defects caused by easter and decapentaplegic (dpp) mutations, but also as dominant zygotic enhancers of dpp alleles for phenotypes in wing. The vri gene encodes a new member of the bZIP family of transcription factors closely related to gene 9 of Xenopus laevis, induced by thyroid hormone during the tadpole tail resorption program, and NF-IL3A, a human T cell transcription factor that transactivates the interleukin-3 promoter. NF-IL3A shares 93% similarity and 60% identity with Vri for a stretch of 68 amino acids that includes the bZIP domain. Although all the alleles tested behave like antimorphs, the dominant enhancement is also seen with a nonsense mutation allele that prevents translation of the bZIP domain. Because of the strong dominant enhancement of dpp phenotypes by vri alleles in both embryo and wing, and also the similarity between the wing vein phenotypes caused by the vri and shortvein dpp alleles, we postulate that vri interacts either directly or indirectly with certain components of the dpp (a TGFβ homologue) signal transduction pathway.


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