Glycolytic gene expression in amphibious Acorus calamus L. under natural conditions

1996 ◽  
Vol 178 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Marcel Bucher ◽  
Roland Br�ndle ◽  
Cris Kuhlemeier
2021 ◽  
Vol 130 ◽  
pp. 103529
Author(s):  
Woo-Ram Park ◽  
Da Jung Lim ◽  
Hyunkyu Sang ◽  
Eunae Kim ◽  
Jae-Hak Moon ◽  
...  

1990 ◽  
Vol 10 (2) ◽  
pp. 859-862
Author(s):  
G M Santangelo ◽  
J Tornow

Glycolytic gene expression in Saccharomyces cerevisiae is thought to be activated by the GCR and TUF proteins. We tested the hypothesis that GCR function is mediated by TUF/GRF/RAP binding sites (UASRPG elements). We found that UASRPG-dependent activation of a heterologous gene and transcription of ADH1, TEF1, TEF2, and RP59 were sensitive to GCR1 disruption. GCR is not required for TUF/GRF/RAP expression or in vitro DNA-binding activity.


1995 ◽  
Vol 15 (5) ◽  
pp. 2646-2653 ◽  
Author(s):  
K Nishi ◽  
C S Park ◽  
A E Pepper ◽  
G Eichinger ◽  
M A Innis ◽  
...  

The GCR1 gene product is required for maximal transcription of yeast glycolytic genes and for growth of yeast strains in media containing glucose as a carbon source. Dominant mutations in two genes, SGC1 and SGC2, as well as recessive mutations in the SGC5 gene were identified as suppressors of the growth and transcriptional defects caused by a gcr1 null mutation. The wild-type and mutant alleles of SGC1 were cloned and sequenced. The predicted amino acid sequence of the SGC1 gene product includes a region with substantial similarity to the basic-helix-loop-helix domain of the Myc family of DNA-binding proteins. The SGC1-1 dominant mutant allele contained a substitution of glutamine for a highly conserved glutamic acid residue within the putative basic DNA binding domain. A second dominant mutant, SGC1-2, contained a valine-for-isoleucine substitution within the putative loop region. The SGC1-1 dominant mutant suppressed the GCR1 requirement for enolase, glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate kinase, phosphoglycerate mutase, and pyruvate kinase gene expression. Expression of the yeast enolase genes was reduced three- to fivefold in strains carrying an sgc1 null mutation, demonstrating that SGC1 is required for maximal enolase gene expression. Expression of the enolase genes in strains carrying gcr1 and sgc1 double null mutations was substantially less than observed for strains carrying either null mutation alone, suggesting that GCR1 and SGC1 function on parallel pathways to activate yeast glycolytic gene expression.


1990 ◽  
Vol 10 (2) ◽  
pp. 859-862 ◽  
Author(s):  
G M Santangelo ◽  
J Tornow

Glycolytic gene expression in Saccharomyces cerevisiae is thought to be activated by the GCR and TUF proteins. We tested the hypothesis that GCR function is mediated by TUF/GRF/RAP binding sites (UASRPG elements). We found that UASRPG-dependent activation of a heterologous gene and transcription of ADH1, TEF1, TEF2, and RP59 were sensitive to GCR1 disruption. GCR is not required for TUF/GRF/RAP expression or in vitro DNA-binding activity.


2012 ◽  
Vol 53 (10) ◽  
pp. 1720-1727 ◽  
Author(s):  
Yosuke Tabei ◽  
Katsuhiko Okada ◽  
Eisuke Horii ◽  
Mayuka Mitsui ◽  
Yoshiaki Nagashima ◽  
...  

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Soyeon Lim ◽  
You-Joung Kim ◽  
Sooyeon Park ◽  
Ji-heon Choi ◽  
Younghoon Sung ◽  
...  

Retinal progenitor cells (RPCs) divide in limited numbers to generate the cells comprising vertebrate retina. The molecular mechanism that leads RPC to the division limit, however, remains elusive. Here, we find that the hyperactivation of mechanistic target of rapamycin complex 1 (mTORC1) in an RPC subset by deletion of tuberous sclerosis complex 1 (Tsc1) makes the RPCs arrive at the division limit precociously and produce Müller glia (MG) that degenerate from senescence-associated cell death. We further show the hyperproliferation of Tsc1-deficient RPCs and the degeneration of MG in the mouse retina disappear by concomitant deletion of hypoxia-induced factor 1-a (Hif1a), which induces glycolytic gene expression to support mTORC1-induced RPC proliferation. Collectively, our results suggest that, by having mTORC1 constitutively active, an RPC divides and exhausts mitotic capacity faster than neighboring RPCs, and thus produces retinal cells that degenerate with aging-related changes.


1996 ◽  
Vol 19 (3) ◽  
pp. 641-642 ◽  
Author(s):  
Eckhard Boles ◽  
Susanne Müller ◽  
Friedrich K. Zimmermann

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