PubMed Health⌕ Search

Biomedical subjects

K Noben-Trauth

Publications and source records attributed to K Noben-Trauth.

23 records · Page 2Linked to original sources
PubMed1996

Expression of B-Myb during mouse embryogenesis.

B-myb is a member of the myb family of nuclear sequence-specific DNA-binding proteins which has been highly conserved among vertebrates. B-myb has been implicated in the control of cell proliferation, particularly at the G1/S transition of the cell cycle. So far, most of the work on B-myb has been performed in immortalized cell lines. Since these cells might show aberrant behavior of genes involved in proliferation control we have begun to investigate the role of B-myb in normal cells. As a first step, we have studied the expression of B-myb during mouse development. Here, we show the B-myb is expressed at similar levels during all stages of embryogenesis. In situ hybridization reveals a tight linkage between B-myb expression and proliferative activity (as assessed by the expression of the S-phase specific histone H4 gene) in most tissues and throughout embryonic development. However, B-myb and histone H4 expression are uncoupled during spermatogenesis in the adult mouse. Histone H4 is expressed at high levels in the early spermatogenic progenitor cells but not in successive stages of sperm cell development. By contrast, the highest levels of B-myb expression are found during the intermediate stages of spermatogenesis. Furthermore, we have found that B-myb mRNA isolated from the testis differs in size from that of other tissues. The data presented here strongly support the notion that B-myb plays a general role during proliferation of most cells. Furthermore, our results raise the possibility that the function of B-myb in cells undergoing meiosis may be different from its role in cells dividing mitotically.

Animals↗
PubMed1996

A candidate gene for the mouse mutation tubby.

A mutation in the tub gene causes maturity-onset obesity, insulin resistance, and sensory deficits. In contrast to the rapid juvenile-onset weight gain seen in diabetes (db) and obese (ob) mice, obesity in tubby mice develops gradually, and strongly resembles the late-onset obesity seen in the human population. Excessive deposition of adipose tissue eventually leads to a twofold increase of body weight. Tubby mice also suffer retinal degeneration and neurosensory hearing loss. The tripartite character of the tubby phenotype shows striking similarity to human obesity syndromes, such as Alström and Bardet-Biedl. Here we report the identification of a G --> T transversion in a candidate gene that abolishes a donor splice site in the 3' coding region and results in a larger transcript containing the unspliced intron. This alteration is predicted to replace the 44-carboxyterminal amino acids with a 20-amino-acid sequence not found in the wide-type protein. Additionally, a second, prematurely truncated transcript with the unspliced intron is observed in testis messenger RNA and a 2-3-fold increase in brain mRNA is observed in tubby mice compared to B6. The phenotype features of tubby mice may be the result of cellular apoptosis triggered by expression of the mutuated tub gene.

Adaptor Proteins, Signal Transducing↗
PubMed1995

Differential splicing of the mouse B-myb gene.

The myb gene family consists of three members, the c-myb proto-oncogene and two myb-related genes (A-myb and B-myb), all of which encode nuclear DNA-binding proteins. Unlike c-myb, which plays a critical role in hematopoietic cells, B-myb is expressed in a large spectrum of hematopoietic as well as non-hematopoietic cells and has been implicated in the control of cell proliferation. The isolation of B-myb cDNA clones from several species has shown that B-myb shares limited homology to the so-called exon 9A of the c-myb gene. This exon is involved in differential splicing as only a subfraction of c-myb mRNA contains exon 9A sequences. The presence in the B-myb cDNA of a sequence related to the exon 9A of c-myb has prompted us to investigate whether B-myb mRNA is also spliced differentially. We here show that B-myb mRNAs containing or lacking exon 9A related sequences are present in many cell types. In contrast to c-myb, where RNA containing the exon 9A constitutes only a minor mRNA fraction, B-myb RNA containing the exon 9A related sequences is the major mRNA form. The proteins encoded by the two B-myb mRNA species are unable to activate promoters to which they bind. Curiously, both B-myb proteins differ in their ability to activate the HSP70 promoter by a myb binding-site independent mechanism; B-myb protein containing exon 9A related aminoacid sequences activates the HSP70 promoter much more potently than the B-myb protein which lacks these sequences. Our results suggest that differential splicing may be a general feature of the members of the myb family and provide first evidence for functional differences of the splice variants.

Amino Acid Sequence↗
PubMed1995

Expression of mouse c-myb during embryonic development.

Three members of the myb gene family, designated as A-myb, B-myb, and c-myb, have been described in many vertebrates. A large body of evidence indicates that the c-myb gene is essential for the development of most hematopoietic lineages. By contrast, the functions of A-myb and B-myb are less well understood. To further explore the relationship between the different myb family members we have compared the expression of A-myb and c-myb during mouse embryogenesis by Northern blotting and by in situ hybridization. In accordance with the important role of c-myb in the hematopoietic system, we detect high levels of c-myb expression in hematopoietic organs such as the fetal liver and the thymus. Surprisingly, we find that high levels of c-myb expression are not restricted to hematopoietic cells. We show that c-myb is strongly expressed in the neural retina and in epithelia of the respiratory tract. The side-by side analysis of c-myb and A-myb expression clearly shows that both genes are expressed in different, but overlapping sets of tissues. Our results suggest that the function of c-myb may not be restricted to hematopoietic cells.

Animals↗