scholarly journals Arabidopsis SUC1 loads the phloem in suc2 mutants when expressed from the SUC2 promoter

2011 ◽  
Vol 63 (2) ◽  
pp. 669-679 ◽  
Author(s):  
Kathrin Wippel ◽  
Norbert Sauer
Keyword(s):  
Suc2 Promoter

Analysis of SUC2 Promoter Structure by Nucleosome Scanning

2011 ◽  
pp. 321-333 ◽  
Author(s):  
Jennifer Chang ◽  
Ales Vancura
Keyword(s):  
Promoter Structure ◽  
Suc2 Promoter

Effects of GAL10-SUC2 promoter combinations on SUC2 gene expression in S. cerevisiae

1993 ◽  
Vol 13 (2) ◽  
pp. 77-83
Author(s):  
Feng Bo ◽  
Li Yu-yang ◽  
Chen Zhao-cong
Keyword(s):  
Gene Expression ◽  
Suc2 Promoter ◽  
Suc2 Gene

scholarly journals A new class of histone H2A mutations in Saccharomyces cerevisiae causes specific transcriptional defects in vivo.

1995 ◽  
Vol 15 (4) ◽  
pp. 1999-2009 ◽  
Author(s):  
J N Hirschhorn ◽  
A L Bortvin ◽  
S L Ricupero-Hovasse ◽  
F Winston
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Activation Function ◽  
Histone H2a ◽  
Yeast Saccharomyces Cerevisiae ◽  
New Class ◽  
Suc2 Promoter ◽  
Encoding Gene ◽  
Transcription Activation Function

Nucleosomes have been shown to repress transcription both in vitro and in vivo. However, the mechanisms by which this repression is overcome are only beginning to be understood. Recent evidence suggests that in the yeast Saccharomyces cerevisiae, many transcriptional activators require the SNF/SWI complex to overcome chromatin-mediated repression. We have identified a new class of mutations in the histone H2A-encoding gene HTA1 that causes transcriptional defects at the SNF/SWI-dependent gene SUC2. Some of the mutations are semidominant, and most of the predicted amino acid changes are in or near the N- and C-terminal regions of histone H2A. A deletion that removes the N-terminal tail of histone H2A also caused a decrease in SUC2 transcription. Strains carrying these histone mutations also exhibited defects in activation by LexA-GAL4, a SNF/SWI-dependent activator. However, these H2A mutants are phenotypically distinct from snf/swi mutants. First, not all SNF/SWI-dependent genes showed transcriptional defects in these histone mutants. Second, a suppressor of snf/swi mutations, spt6, did not suppress these histone mutations. Finally, unlike in snf/swi mutants, chromatin structure at the SUC2 promoter in these H2A mutants was in an active conformation. Thus, these H2A mutations seem to interfere with a transcription activation function downstream or independent of the SNF/SWI activity. Therefore, they may identify an additional step that is required to overcome repression by chromatin.

scholarly journals Efficiency of graft-transmitted JcFT for floral induction in woody perennial species of the Jatropha genus depends on transport distance

2021 ◽  
Author(s):  
Mingyong Tang ◽  
Xue Bai ◽  
Jingxian Wang ◽  
Tao Chen ◽  
Xin Meng ◽  
...  
Keyword(s):  
Floral Induction ◽  
Protein Abundance ◽  
Perennial Species ◽  
Wild Type ◽  
Flowering Locus T ◽  
Genetic Pathways ◽  
Woody Perennials ◽  
Woody Perennial ◽  
Transport Distance ◽  
Suc2 Promoter

Abstract Flowering Locus T (FT) promotes flowering by integrating six genetic pathways. In Arabidopsis, the FT protein is transported from leaves to shoot apices and induces flowering. However, contradictory conclusions about floral induction via graft-transmitted FT in trees were reported in previous studies. We obtained extremely early-flowering transgenic woody Jatropha curcas by overexpression of J. curcas FT using Arabidopsis thaliana SUC2 promoter (SUC2:JcFT) and non-flowering transgenic J. curcas by RNA interference (RNAi), which were used to investigate the function of graft-transmitted JcFT in floral induction in woody perennials. Scions from five wild-type species of the Jatropha genus and from JcFT-RNAi transgenic J. curcas were grafted onto SUC2:JcFT rootstocks. Most grafted plants produced flowers in 1–2 months, and the flowering percentage and frequency of various grafted plants decreased with increasing scion length. Consistently, FT protein abundance in scions also decreased with increasing distance from graft junctions to the buds. These findings suggest that FT proteins can be transmitted by grafting and can induce the floral transition in woody perennials, and the efficiency of graft-transmitted JcFT for floral induction depends on the scion length, which may help explain previous seemingly contradictory observations regarding floral induction via graft-transmitted FT in trees.

scholarly journals Control of Gene Expression from the SUC2 Promoter of Saccharomyces cerevisiae using Two Carbon Sources.

1992 ◽  
Vol 18 (5) ◽  
pp. 693-700 ◽  
Author(s):  
Takayuki Ohshima ◽  
Xiao-Li Zhang ◽  
Shinji Iijima ◽  
Takeshi Kobayashi ◽  
Fumio Hishinuma
Keyword(s):  
Gene Expression ◽  
Saccharomyces Cerevisiae ◽  
Carbon Sources ◽  
Control Of Gene Expression ◽  
Suc2 Promoter

Enhancement, by succinate addition, of the production of cloned glucoamylase from recombinant yeast using a SUC2 promoter

1998 ◽  
Vol 33 (3) ◽  
pp. 257-261 ◽  
Author(s):  
Hyung Joon Cha ◽  
Min-Hong Kim ◽  
Sung Hong Kim ◽  
Joo Sang Yeo ◽  
Hee Jeong Chae ◽  
...  
Keyword(s):  
Recombinant Yeast ◽  
Suc2 Promoter

scholarly journals Synergistic release from glucose repression by mig1 and ssn mutations in Saccharomyces cerevisiae.

Genetics ◽  
1994 ◽  
Vol 137 (1) ◽  
pp. 49-54 ◽  
Author(s):  
L G Vallier ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Protein Kinase ◽  
Dna Binding ◽  
Glucose Repression ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Yeast Saccharomyces Cerevisiae ◽  
Suc2 Promoter ◽  
Repressor Complex ◽  
Glucose Availability

Abstract In the yeast Saccharomyces cerevisiae, glucose repression of SUC2 transcription requires the SSN6-TUP1 repressor complex. It has been proposed that the DNA-binding protein MIG1 secures SSN6-TUP1 to the SUC2 promoter. Here we show that a mig1 deletion does not cause nearly as dramatic a loss of repression as ssn6: glucose-grown mig1 mutants display 20-fold lower SUC2 expression than ssn6 mutants. Thus, repression by SSN6-TUP1 is not mediated solely by MIG1, but also involves MIG1-independent mechanisms. We report that mig1 partially restores SUC2 expression in mutants lacking the SNF1 protein kinase and show that mig1 is allelic to ssn1, a mutation selected as a suppressor of snf1. Other SSN genes identified in this selection were therefore candidates for a role in repression of SUC2. We show that mig1 acts synergistically with ssn2 through ssn5, ssn7, and ssn8 to relieve glucose repression of SUC2 and to suppress the requirement for SNF1. These findings indicate that the SSN proteins contribute to repression of SUC2, and the pleiotropic phenotypes of the ssn mutants suggest global roles in repression. Finally, the regulated SUC2 expression observed in snf1 mig1 mutants indicates that signals regarding glucose availability can be transmitted independently of the SNF1 protein kinase.

Enhancement of secreted production of glucoamylase through fed-batch bioreactor culture of recombinant yeast harboring glucose-controllable SUC2 promoter

2007 ◽  
Vol 24 (5) ◽  
pp. 812-815 ◽  
Author(s):  
Hyung Joon Cha ◽  
Kyoung Ro Kim ◽  
Byeong Hee Hwang ◽  
Dae Hee Ahn ◽  
Young Je Yoo
Keyword(s):  
Bioreactor Culture ◽  
Recombinant Yeast ◽  
Fed Batch ◽  
Batch Bioreactor ◽  
Suc2 Promoter
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