scholarly journals Antisense Expression of the CK2 α-Subunit Gene in Arabidopsis. Effects on Light-Regulated Gene Expression and Plant Growth

1999 ◽  
Vol 119 (3) ◽  
pp. 989-1000 ◽  
Author(s):  
Yew Lee ◽  
Alan M. Lloyd ◽  
Stanley J. Roux
1994 ◽  
Vol 45 (3) ◽  
pp. 672-678 ◽  
Author(s):  
Pilar Bofill ◽  
I. Annelise Goecke ◽  
Silvia Bonilla ◽  
Miriam Alvo ◽  
Elisa T. Marusic

2001 ◽  
Vol 120 (5) ◽  
pp. A308-A308
Author(s):  
S KUSAYANAGI ◽  
Y TAKEUCHI ◽  
K MITAMURA ◽  
A TODISCO

2021 ◽  
Author(s):  
Wentao Wang ◽  
Yue Lu ◽  
Junjie Li ◽  
Xinran Zhang ◽  
Fangfang Hu ◽  
...  

Abstract Plant SNF1-Related Kinase1 (SnRK1) is an evolutionarily conserved energy-sensing protein kinase that orchestrates transcriptional networks to maintain cellular energy homeostasis when energy supplies become limited. However, the mechanism by which SnRK1 regulates this gene expression switch to gauge cellular energy status remains largely unclear. In this work, we show that the rice histone H3K27me3 demethylase JMJ705 is required for low energy stress tolerance in rice plants. The genetic inactivation of JMJ705 resulted in similar effects as those of the rice snrk1 mutant on the transcriptome, which impairs not only the promotion of the low energy stress-triggered transcriptional program but also the repression of the program under an energy-sufficient state. We show that the α-subunit of OsSnRK1 interacts with and phosphorylates JMJ705 to stimulate its H3K27me3 demethylase activity. Further analysis revealed that JMJ705 directly targets a set of low energy stress-responsive transcription factor genes. These results uncover the chromatin mechanism of SnRK1-regulated gene expression in both energy-sufficient and -limited states in plants and suggest that JMJ705 functions as an upstream regulator of the SnRK1α-controlled transcriptional network.


1996 ◽  
Vol 15 (1) ◽  
pp. 29-39 ◽  
Author(s):  
Helena C. D'Cotta ◽  
Claudiane Gallais ◽  
Bénédicte Saulier ◽  
Patrick Prunet

1987 ◽  
Vol 115 (3) ◽  
pp. R21-R23 ◽  
Author(s):  
S.R. Davis ◽  
Z. Krozowski ◽  
R.I. McLachlan ◽  
H.G. Burger

ABSTRACT We report inhibin α- and βA -subunit gene expression in the human corpus luteum and placenta using human α-subunit and bovine βA -subunit nucleic acid probes. In addition, we have demonstrated the presence of immunoreactive and bioactive inhibin in human corpora lutea. Our findings suggest that this tissue is a significant source of inhibin during the luteal phase of the normal human menstrual cycle.


1994 ◽  
Vol 162 (1) ◽  
pp. 259-266 ◽  
Author(s):  
Daniel J. MacPhee ◽  
Kevin J. Barr ◽  
Paul A. De Sousa ◽  
Stanley D.L. Todd ◽  
Gerald M. Kidder

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 4168-4176 ◽  
Author(s):  
C. Glidewell-Kenney ◽  
J. Weiss ◽  
L. A. Hurley ◽  
J. E. Levine ◽  
J. L. Jameson

Estrogen, acting via estrogen receptor (ER)α, regulates serum gonadotropin levels and pituitary gonadotropin subunit expression. However, the cellular pathways mediating this regulation are unknown. ERα signals through classical estrogen response element (ERE)-dependent genomic as well as nonclassical ERE-independent genomic and nongenomic pathways. Using targeted mutagenesis in mice to disrupt ERα DNA binding activity, we previously demonstrated that ERE-independent signaling is sufficient to suppress serum LH levels. In this study, we examined the relative roles of ERE-dependent and -independent estrogen signaling in estrogen regulation of LH, FSH, prolactin, and activin/inhibin subunit gene expression, pituitary LH and FSH protein content, and serum FSH levels. ERE-independent signaling was not sufficient for estrogen to induce pituitary prolactin mRNA or suppress pituitary LHβ mRNA, LH content, or serum FSH in estrogen-treated ovariectomized mice. However, ERE-independent signaling was sufficient to reduce pituitary glycoprotein hormone α-subunit, FSHβ, and activin-βB mRNA expression. Together with previous serum LH results, these findings suggest ERE-independent ERα signaling suppresses serum LH via reduced secretion, not synthesis. Additionally, ERE-dependent and ERE-independent ERα pathways may distinctly regulate steps involved in the synthesis and secretion of FSH.


1986 ◽  
Vol 70 (s13) ◽  
pp. 16P-16P
Author(s):  
J.A. Franklyn ◽  
D.F. Wood ◽  
T.C. Lynam ◽  
D.B. Ramsden ◽  
K. Docherty ◽  
...  

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