Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-1868
Lichtlen, P; Georgiev, O; Schaffner, W; Aguzzi, A; Brandner, S (1999). The heavy metal-responsive transcription factor-1 (MTF-1) is not required for neural differentiation. Biological Chemistry, 380(6):711-715.
View at publisher
The zinc finger transcription factor MTF-1 is essential for proper response to heavy metal load and other stress conditions in vertebrates, and also contributes to the maintenance of the cellular redox state. Target genes include metallothioneins (MT-I and MT-II) and gamma-glutamylcysteine synthetase (gamma-GCS), an enzyme involved in glutathione biosynthesis. Although MTF-1 is expressed ubiquitously, the primary defect in null mutant mice is hepatocyte necrosis, which results in embryonic lethality around day E14 and prevents the analysis of delayed effects on other organs. To assess the impact of MTF-1 deficiency on the function of the mature central nervous system, we employed the neural grafting strategy. Neuroectodermal brain tissue obtained from transgenic mouse embryos at gestational day 12.5 was transplanted into the caudoputamen of adult wild-type mice. 33 days later, grafts derived from MTF-1 deficient mice consisted of fully differentiated neuroectodermal tissue and showed no differences to heterozygous control grafts. This indicates that MTF-1 is dispensable for the development and differentiation of the nervous system. Such transplants devoid of MTF-1 may provide a useful tool for the further investigation of the effect of cell stress, including oxidative stress.
107 downloads since deposited on 11 Feb 2008
21 downloads since 12 months
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology|
|Dewey Decimal Classification:||570 Life sciences; biology
610 Medicine & health
|Date:||1 June 1999|
|Deposited On:||11 Feb 2008 12:26|
|Last Modified:||05 Apr 2016 12:20|
Users (please log in): suggest update or correction for this item
Repository Staff Only: item control page