Embryonic Liver Degeneration and Increased Sensitivity Towards Heavy Metal and H2O2 in Mice Lacking the Metal-Responsive Transcription Factor MTF-1

1999 ◽  
pp. 339-352
Author(s):  
Peter Lichtlen ◽  
Çagatay Günes ◽  
Rainer Heuchel ◽  
Oleg Georgiev ◽  
Karl-Heinz Müller ◽  
...  
2004 ◽  
Vol 385 (7) ◽  
pp. 597-603 ◽  
Author(s):  
K. Balamurugan ◽  
D. Egli ◽  
A. Selvaraj ◽  
B. Zhang ◽  
O. Georgiev ◽  
...  

AbstractThe zinc finger transcription factor MTF-1 (metalresponsive transcription factor-1) is conserved from insects to vertebrates. Its major role in both organisms is to control the transcription of genes involved in the homeostasis and detoxification of heavy metal ions such as Cu[2+], Zn[2+] and Cd [2+]. In mammals, MTF-1 serves at least two additional roles. First, targeted disruption of the MTF-1 gene results in death at embryonic day 14 due to liver degeneration, revealing a stagespecific developmental role. Second, under hypoxicanoxic stress, MTF-1 helps to activate the transcription of the gene placental growth factor (PlGF), an angiogenic protein. Recently we characterized dMTF-1, theDrosophilahomolog of mammalian MTF-1. Here we present a series of studies to compare the metal response in mammals and insects, which reveal common features but also differences. A human MTF-1 transgene can restore to a large extent metal tolerance to flies lacking their own MTF-1 gene, both at low and high copper concentrations. Likewise,DrosophilaMTF-1 can substitute for human MTF-1 in mammalian cell culture, although both the basal and the metalinduced transcript levels are lower. Finally, a clear difference was revealed in the response to mercury, a highly toxic heavy metal: metallothioneintype promoters respond poorly, if at all, to Hg[2+] in mammalian cells but strongly inDrosophila, and this response is completely dependent on dMTF-1.


2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Fangwei Yu ◽  
Shenyun Wang ◽  
Wei Zhang ◽  
Hong Wang ◽  
Li Yu ◽  
...  

Abstract The members of myeloblastosis transcription factor (MYB TF) family are involved in the regulation of biotic and abiotic stresses in plants. However, the role of MYB TF in phosphorus remobilization remains largely unexplored. In the present study, we show that an R2R3 type MYB transcription factor, MYB103, is involved in phosphorus (P) remobilization. MYB103 was remarkably induced by P deficiency in cabbage (Brassica oleracea var. capitata L.). As cabbage lacks the proper mutant for elucidating the mechanism of MYB103 in P deficiency, another member of the crucifer family, Arabidopsis thaliana was chosen for further study. The transcript of its homologue AtMYB103 was also elevated in response to P deficiency in A. thaliana, while disruption of AtMYB103 (myb103) exhibited increased sensitivity to P deficiency, accompanied with decreased tissue biomass and soluble P concentration. Furthermore, AtMYB103 was involved in the P reutilization from cell wall, as less P was released from the cell wall in myb103 than in wildtype, coinciding with the reduction of ethylene production. Taken together, our results uncover an important role of MYB103 in the P remobilization, presumably through ethylene signaling.


2003 ◽  
Vol 279 (6) ◽  
pp. 4515-4522 ◽  
Author(s):  
Xiaohua Chen ◽  
Bo Zhang ◽  
Philip M. Harmon ◽  
Walter Schaffner ◽  
David O. Peterson ◽  
...  

mSphere ◽  
2018 ◽  
Vol 3 (5) ◽  
Author(s):  
Yonglin Wang ◽  
Chenglin Deng ◽  
Longyan Tian ◽  
Dianguang Xiong ◽  
Chengming Tian ◽  
...  

ABSTRACT Iron homeostasis is essential for full virulence and viability in many pathogenic fungi. Here, we showed that the bZip transcription factor VdHapX functions as a key regulator of iron homeostasis for adaptation to iron-depleted and iron-excess conditions and is required for full virulence in the vascular wilt fungus, Verticillium dahliae. Deletion of VdHapX impaired mycelial growth and conidiation under both iron starvation and iron sufficiency. Furthermore, disruption of VdHapX led to decreased formation of the long-lived survival structures of V. dahliae, known as microsclerotia. Expression of genes involved in iron utilization pathways and siderophore biosynthesis was misregulated in the ΔVdHapX strain under the iron-depleted condition. Additionally, the ΔVdHapX strain exhibited increased sensitivity to high iron concentrations and H2O2, indicating that VdHapX also contributes to iron or H2O2 detoxification. The ΔVdHapX strain showed a strong reduction in virulence on smoke tree seedlings (Cotinus coggygria) and was delayed in its ability to penetrate plant epidermal tissue. IMPORTANCE This study demonstrated that VdHapX is a conserved protein that mediates adaptation to iron starvation and excesses, affects microsclerotium formation, and is crucial for virulence of V. dahliae.


2018 ◽  
Vol 114 (suppl_1) ◽  
pp. S15-S15
Author(s):  
A Akhmedov ◽  
F Montecucco ◽  
A Schaub Clerigue ◽  
S Costantino ◽  
F Paneni ◽  
...  

2006 ◽  
Vol 84 (10) ◽  
pp. 1029-1041 ◽  
Author(s):  
Caroline Morin ◽  
Eric Rousseau

The mechanical properties and Ca2+ sensitivity of an organ-culture model derived from guinea pig airways have been examined. The cultured explants develop airway hyperresponsiveness to pharmacological agonists after 3-day culture, when compared with fresh and ovalbumin-sensitized tissues. The reactivity of cultured explants is dependent on the presence of the epithelium. They are also sensitive to glucocorticosteroid pretreatments, which neutralize the TNFα antibody and ΝF-κB inhibitor. Hence, specific immunostaining of ΝF-κB subunits (p65 and p50) was increased in the nuclear extract of cultured explants. In β-escin-permeabilized preparations, step-increases in pCa revealed enhanced Ca2+ sensitivity of the contractile apparatus in cultured explants, which was prevented by epithelium removal. Pretreatments of cultured explants with neutralizing TNFα antibody and ΝF-κB inhibitor consistently reduced their Ca2+ sensitivity. These findings suggest that AHR developed in this organ culture model may be triggered by an inflammatory process mediated by the TNFα and NF-κB transcription factor, which results in an increased sensitivity to [Ca2+]i.


Sign in / Sign up

Export Citation Format

Share Document