Importance of leucine zipper domain of mi transcription factor (MITF) for differentiation of mast cells demonstrated using mi(ce)/mi(ce) mutant mice of which MITF lacks the zipper domain.

@article{Morii2001ImportanceOL,
  title={Importance of leucine zipper domain of mi transcription factor (MITF) for differentiation of mast cells demonstrated using mi(ce)/mi(ce) mutant mice of which MITF lacks the zipper domain.},
  author={Eiichi Morii and Hideki Ogihara and D. K. Kim and Akihiko Ito and Keisuke Oboki and Y. M. Lee and Tomoko Jippo and Shintaro Nomura and Kazutaka Maeyama and M. Lynn Lamoreux and Yukihiko Kitamura},
  journal={Blood},
  year={2001},
  volume={97 7},
  pages={
          2038-44
        }
}
The mi transcription factor (MITF) is a basic helix-loop-helix leucine zipper (bHLH-Zip) transcription factor that is important for the development of mast cells. Mast cells of mi/mi genotype express normal amount of abnormal MITF (mi-MITF), whereas mast cells of tg/tg genotype do not express any MITFs. Mast cells of mi/mi mice show more severe abnormalities than those of tg/tg mice, indicating that the mi-MITF possesses the inhibitory function. The MITF encoded by the mi(ce) mutant allele (ce… 
View on PubMed
bloodjournal.org
32 Citations
Highly Influential Citations
1
Background Citations
4

Figures and Tables from this paper

32 Citations

Citation Type

Citation Type

Effect of a large deletion of the basic domain of mi transcription factor on differentiation of mast cells.
TLDR
In mi(ew)/mi(ew) CMCs, the expression pattern of genes whose transcription was affected by MITF was comparable to that of tg/tg CMC’s rather than that of mi/mi C MCs, suggesting that ew-MITF lacked any functions, and the effect of a large deletion of the basic domain was examined.
Inhibitory effect of the mi transcription factor encoded by the mutant mi allele on GA binding protein-mediated transcript expression in mouse mast cells.
TLDR
This is the first study to show that expression of an abnormal form of a bHLH-Zip transcription factor can dramatically alter the intracellular location of another DNA/RNA binding factor, which in turn brings about profound and unexpected consequences on transcript expression.
Dual abnormal effects of mutant MITF encoded by Mi(wh) allele on mouse mast cells: decreased but recognizable transactivation and inhibition of transactivation.
Interaction and Cooperation of mi Transcription Factor (MITF) and Myc-associated Zinc-finger Protein-related Factor (MAZR) for Transcription of Mouse Mast Cell Protease 6 Gene*
TLDR
MAZR appeared to play important roles in the normal phenotypic expression of mast cells in association with MITF, indicating that the MAZR and MITF synergistically transactivated the mMCP-6 gene.
Additive effect of mouse genetic background and mutation of MITF gene on decrease of skin mast cells.
TLDR
The mi/mi mutant mice showed a significant decrease of skin mast cells in C57BL/6 (B6) genetic background but not in WB genetic background, suggesting that a factor compensating the reduced expression of KIT was present in WB-mi/mi mice.
Effect of MITF on mast cell differentiation.
Number of mast cells in the peritoneal cavity of mice: influence of microphthalmia transcription factor through transcription of newly found mast cell adhesion molecule, spermatogenic immunoglobulin superfamily.
Strain-dependent inhibitory effect of mutant mi-MITF on cytotoxic activities of cultured mast cells and natural killer cells of mice
TLDR
WB-mi/mi mice appeared to have factor(s) compensating for the inhibitory effect of mi-MITF on the expression of Gr B and Pfn genes, and cytotoxic activities of CMCs and NK cells were not impaired in WB-mi-mi mice.
Failure to Target RANKL Signaling Through p38‐MAPK Results in Defective Osteoclastogenesis in the Microphthalmia Cloudy‐Eyed Mutant
TLDR
It is shown that the Mitfce allele leads to a dense bone phenotype in neonatal mice due to defective osteoclast differentiation, and the crucial role of signaling dependent MITF/p38 MAPK interactions in osteOClast differentiation is highlighted.
Role of MITF for Mast Cell Differentiation Analyzed by Skin and Bone Marrow Transplantations
TLDR
Investigation of the abnormalities of mast cell precursors and environment in tg/tg mice by skin and bone marrow transplantations showed that the tissue environment for mast cell development was defective in tG/TG mice, indicating that MITF was essential for both mast cell precursor and tissue environment.
...
1
2
3
4
...

References

SHOWING 1-10 OF 61 REFERENCES
Involvement of transcription factor encoded by the mi locus in the expression of c-kit receptor tyrosine kinase in cultured mast cells of mice.
TLDR
The involvement of (+)-MITF in the c-kit transactivation appeared to be specific to the mast cell lineage.
Involvement of transcription factor encoded by the mouse mi locus (MITF) in expression of p75 receptor of nerve growth factor in cultured mast cells of mice.
TLDR
Overexpression of +- MITF but not of mi-MITF normalized the expression of p75 and the above-mentioned poor responses of mi/mi CMCs to NGF, indicating the involvement of + -MITF in p75 gene transactivation.
Inhibitory effect of the transcription factor encoded by the mi mutant allele in cultured mast cells of mice.
TLDR
The results indicated the inhibitory effect of mi -MITF on the transactivation of particular genes in CMCs, and compared mRNA expression of six genes between mi/mi and tg/tg C MCs by Northern analysis.
Involvement of mi-Transcription Factor in Expression of α-Melanocyte-Stimulating Hormone Receptor in Cultured Mast Cells of Mice1 2
TLDR
Results indicated that +-MITF directly transactivated the MC1R gene through these two motifs, and that mi/mi CMCs did not express a receptor (MC1R) for α-melanocyte-stimulating hormone.
Involvement of transcription factor encoded by the mouse mi locus (MITF) in apoptosis of cultured mast cells induced by removal of interleukin-3.
TLDR
The (+)-MITF appeared to play some roles for the acceleration of the apoptosis specifically in the mast cell lineage, as the apoptotic process proceeded faster in +/+ C MCs than in mi/mi CMCs.
Systematic method to obtain novel genes that are regulated by mi transcription factor: impaired expression of granzyme B and tryptophan hydroxylase in mi/mi cultured mast cells.
TLDR
To obtain new genes whose transcription may be regulated by MITF, a subtracted cDNA library was prepared using +/+ and mi/mi CMCs and the +-MITF bound three and one CANNTG motifs in the Gr B and TPH promoters, respectively, and transactivated these two genes, indicating the involvement of MITF in their expression.
Different effect of various mutant MITF encoded by mi, Mior, or Miwh allele on phenotype of murine mast cells.
TLDR
The rank order of mast cell abnormality appears to be related to the functional abnormality of MITF encoded by each mutant gene, and the potential was significantly impaired in mi-MITF.
Deficient transcription of mouse mast cell protease 4 gene in mutant mice of mi/mi genotype.
TLDR
It is reported that expression of the mouse mast cell protease 5 (MMCP-5) and MMCP-6 genes were deficient in cultured mast cells (CMC) derived from mutant mice of mi/mi genotype, and the regulation mechanisms were different.
Regulation of mouse mast cell protease 6 gene expression by transcription factor encoded by the mi locus.
TLDR
The mi locus of mice encodes a member of the basic-helix-loop-helIX-leucine zipper (bHLH-Zip) protein family of transcription factors (hereafter called MITF), and the effect of MITF on the transcription of the MMCP-6 gene is investigated.
Cell type-specific deficiency of c-kit gene expression in mutant mice of mi/mi genotype.
TLDR
The c-kit expression was deficient in mast cells but not in erythroid precursors, testicular germ cells, and neurons of mi/mi mice, which suggested that the regulation of the c-Kit transcription by the mi factor was dependent on cell types.
...
1
2
3
4
5
...