Feedback mechanism in the chemical ecology of plants: role of soil microorganisms

Author(s):  
X. Carlos Souto ◽  
FranÇois Pellissier
2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
M. K. Gill-Sharma

In the last 20 years, a pituitary-hypothalamus tissue culture system with intact neural and portal connections has been developed in our lab and used to understand the feedback mechanisms that regulate the secretions of adenohypophyseal hormones and fertility of male rats. In the last decade, several in vivo rat models have also been developed in our lab with a view to substantiate the in vitro findings, in order to delineate the role of pituitary hormones in the regulation of fertility of male rats. These studies have relied on both surgical and pharmacological interventions to modulate the secretions of gonadotropins and testosterone. The interrelationship between the circadian release of reproductive hormones has also been ascertained in normal men. Our studies suggest that testosterone regulates the secretion of prolactin through a long feedback mechanism, which appears to have been conserved from rats to humans. These studies have filled in a major lacuna pertaining to the role of prolactin in male reproductive physiology by demonstrating the interdependence between testosterone and prolactin. Systemic levels of prolactin play a deterministic role in the mechanism of chromatin condensation during spermiogenesis.


2015 ◽  
Vol 112 (15) ◽  
pp. 4678-4683 ◽  
Author(s):  
Yu Shi ◽  
Jianquan Chen ◽  
Courtney M. Karner ◽  
Fanxin Long

Hedgehog (Hh) signaling is essential for osteoblast differentiation in the endochondral skeleton during embryogenesis. However, the molecular mechanism underlying the osteoblastogenic role of Hh is not completely understood. Here, we report that Hh markedly induces the expression of insulin-like growth factor 2 (Igf2) that activates the mTORC2-Akt signaling cascade during osteoblast differentiation. Igf2-Akt signaling, in turn, stabilizes full-length Gli2 through Serine 230, thus enhancing the output of transcriptional activation by Hh. Importantly, genetic deletion of the Igf signaling receptor Igf1r specifically in Hh-responding cells diminishes bone formation in the mouse embryo. Thus, Hh engages Igf signaling in a positive feedback mechanism to activate the osteogenic program.


Nephrology ◽  
1984 ◽  
pp. 143-153 ◽  
Author(s):  
Josephine P. Briggs ◽  
Jürgen Schnermann

Author(s):  
Carmelo Gurnari ◽  
Simona Pagliuca ◽  
Yihong Guan ◽  
Vera Adema ◽  
Courtney E Hershberger ◽  
...  

Decrease in DNA dioxygease activity generated by TET2 gene family is crucial in myelodysplastic syndromes (MDS). The general down-regulation of 5-hydroxymethylcytosine (5-hmC) argues for a role of DNA demethylation in MDS beyond TET2 mutations, which albeit frequent, do not convey any prognostic significance. We investigated TETs expression to identify factors which can modulate the impact of mutations and thus 5-hmC levels on clinical phenotypes and prognosis of MDS patients. DNA/RNA-sequencing and 5-hmC data were collected from 1,665 patients with MDS and 91 controls. Irrespective of mutations, a significant fraction of MDS patients exhibited lower TET2 expression, while 5-hmC levels were not uniformly decreased. In searching for factors explaining compensatory mechanisms, we discovered that TET3 was up-regulated in MDS and inversely correlated with TET2 expression in wild-type cases. While TET2 was reduced across all age-groups, TET3 levels were increased in a likely feedback mechanism induced by TET2 dysfunction. This inverse relationship of TET2 and TET3 expression also corresponded to the expression of L-2-hydroxyglutarate dehydrogenase, involved in agonist/antagonist substrate metabolism. Importantly, elevated TET3 levels influenced the clinical phenotype of TET2-deficiency whereby the lack of compensation by TET3 (low TET3 expression) was associated with poor outcomes of TET2 mutant carriers.


2018 ◽  
Vol 156 (5) ◽  
pp. 918-934 ◽  
Author(s):  
QINGFENG MENG ◽  
JOHN HOOKER ◽  
JOE CARTWRIGHT

AbstractBedding-parallel fibrous calcite veins in black shales (Cretaceous, southern UK) were investigated using a combined field, stable isotopic geochemistry, petrographic and crystallographic method to examine their formation mechanism. Calcite veins occur in all shale beds and are most abundant in the bituminous shales of the Chief Beef Beds. The calcite fibres in these veins exhibit either an antitaxial fibre growth with curvy stylolites as the median zone, or a predominantly syntaxial, upwards growth. The calcite veins range from –0.49 to 1.78‰ of δ13C values, and –6.53 to –0.03‰ of δ18O values, which are both similar to those of their host shales. Our petrographic observations demonstrate that subhorizontal and interconnecting microstylolite networks commonly occur within the calcite veins. Equant calcite grains in the median zones exhibit indenting, truncating and also interpenetrating grain contacts. It is interpreted that the fibrous calcite veins were sourced by neomorphic calcite from their host shales, with evidence from the δ13C signatures, pressure-solution features (stylolites, microstylolites and grain contact styles) and embedded fossil ghosts within the veins. The diagenetic fluids, from which calcite was precipitated, were a mixing of the original seawaters and 18O-depleted meteoric waters. Development of bedding-parallel calcite veins is considered to have been enhanced by pressure solution as a positive feedback mechanism, which was facilitated by the overburden pressure as the maximum principal stress. Calcite fibres, with a predominant subvertical c-axis orientation, exhibit a displacive growth in porous shales and a replacive growth at vein-limestone contacts. This study highlights the critical role of pressure solution in the formation of bedding-parallel calcite veins during burial and diagenesis of immature black shales.


2019 ◽  
Vol 316 (6) ◽  
pp. E987-E997 ◽  
Author(s):  
Binbin Huang ◽  
Chen Huang ◽  
Huashan Zhao ◽  
Wen Zhu ◽  
Baobei Wang ◽  
...  

Chemerin and G protein-coupled receptor 1 (GPR1) are increased in serum and placenta in mice during pregnancy. Interestingly, we observed increased serum chemerin levels and decreased GPR1 expression in placenta of high-fat-diet-fed mice compared with chow-fed mice at gestational day 18. GPR1 protein and gene levels were significantly decreased in gestational diabetes mellitus (GDM) patient placentas. Therefore, we hypothesized that chemerin/GPR1 signaling might participate in the pathogenic mechanism of GDM. We investigated the role of GPR1 in carbohydrate homeostasis during pregnancy using pregnant mice transfected with small interfering RNA for GPR1 or a negative control. GPR1 knockdown exacerbated glucose intolerance, disrupted lipid metabolism, and decreased β-cell proliferation and insulin levels. Glucose transport protein-3 and fatty acid binding protein-4 were downregulated with reducing GPR1 in vivo and in vitro via phosphorylated AKT pathway. Taken together, our findings first demonstrate the expression of GPR1, the characterization of its direct biological effects in humans and mice, as well as the molecular mechanism that indicates the role of GPR1 signaling in maternal metabolism during pregnancy, suggesting a novel feedback mechanism to regulate glucose balance during pregnancy, and GPR1 could be a potential target for the detection and therapy of GDM.


1997 ◽  
Vol 272 (4) ◽  
pp. C1178-C1185 ◽  
Author(s):  
L. Garcia ◽  
M. Fahmi ◽  
N. Prevarskaya ◽  
B. Dufy ◽  
P. Sartor

In pituitary cells, voltage-dependent Ca2+ channels play an important role in such physiological processes as exocytosis, secretion, the cell cycle, and proliferation. Thus mechanisms that modulate voltage-dependent Ca2+ channel activity participate indirectly in regulating intracellular Ca2+ concentration. We have shown a new modulating mechanism for voltage-dependent Ca2+ channels by demonstrating that Ca2+ influx is influenced by Cl-. To evaluate the role of Cl- on Ca2+ conductance coupling, we first measured the intracellular Cl- concentration of rat lactotrophs using the Cl(-)-sensitive fluorescence probe sulfopropylquinolinium by simple microspectrofluorometry or combined with electrophysiology. We found an average intracellular Cl- concentration of rat lactotrophs of approximately 60 mM (n = 39). Using the whole cell tight-seal recording technique, we showed that a reduction in external Cl- concentration ([Cl-]o) and a decrease in Cl- conductances affected Ca2+ conductance as measured by Ba2+ movement through the Ca2+ channels (I(Ba)). Low [Cl-]o (39 mM) induced a decrease in Ca2+ entry via voltage-gated Ca2+ channels (-27.75 +/- 4% of normalized I(Ba)). Similarly, blockade of the Cl- conductance by 1 mM 9-anthracene carboxylic acid induced a decrease in I(Ba) (-26 +/- 6% of normalized I(Ba)). This modulation of I(Ba) was inhibited by 24-h pretreatment of the cells with pertussis toxin (1 microg/ml), suggesting that changes in Cl- concentration induced by low [Cl-]o and 9-anthracene carboxylic acid interfered with the phosphorylation of G proteins involved in Ca2+ channel activation. These results suggest a feedback mechanism based on constant interaction between Ca2+ and Cl-. Finally, they also emphasize the physiological role of Cl- in rat lactotrophs.


1979 ◽  
Vol 55 (6) ◽  
pp. 776-786
Author(s):  
Masatomo MORI ◽  
Kihachi OHSHIMA ◽  
Sakae MARUTA ◽  
Hitoshi FUKUDA ◽  
Yohnosuke SHIMOMURA ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document