Comparison of the neuralized genes of Drosophila virilis and D. melanogaster

Genome ◽  
1994 ◽  
Vol 37 (5) ◽  
pp. 840-847 ◽  
Author(s):  
Lily Zhou ◽  
Gabrielle L. Boulianne

The neurogenic gene neuralized of Drosophila melanogaster is thought to play a role in the determination of cell fate in the embryonic nervous system as well as other tissues during development. To determine which sequences within the neuralized gene encode functionally important domains, we have initiated an interspecific comparison of the neuralized gene of D. virilis and D. melanogaster. In this study we show that several motifs that we have previously identified in the neuralized protein of D. melanogaster are conserved in D. virilis. These include a putative nuclear localization signal, a homeodomain similarity region, and a zinc finger motif. In contrast, a helix-turn-helix motif with structural similarity to those identified as DNA-binding regions of bacterial repressors is deleted. These results demonstrate that it is possible to identify key functional regions of the neuralized protein by an interspecific comparison.Key words: Drosophila melanogaster, Drosophila virilis, neuralized, nucleotide sequence, evolutionary comparison.

Genetics ◽  
2001 ◽  
Vol 157 (3) ◽  
pp. 1387-1395 ◽  
Author(s):  
Sudhir Kumar ◽  
Sudhindra R Gadagkar ◽  
Alan Filipski ◽  
Xun Gu

AbstractGenomic divergence between species can be quantified in terms of the number of chromosomal rearrangements that have occurred in the respective genomes following their divergence from a common ancestor. These rearrangements disrupt the structural similarity between genomes, with each rearrangement producing additional, albeit shorter, conserved segments. Here we propose a simple statistical approach on the basis of the distribution of the number of markers in contiguous sets of autosomal markers (CSAMs) to estimate the number of conserved segments. CSAM identification requires information on the relative locations of orthologous markers in one genome and only the chromosome number on which each marker resides in the other genome. We propose a simple mathematical model that can account for the effect of the nonuniformity of the breakpoints and markers on the observed distribution of the number of markers in different conserved segments. Computer simulations show that the number of CSAMs increases linearly with the number of chromosomal rearrangements under a variety of conditions. Using the CSAM approach, the estimate of the number of conserved segments between human and mouse genomes is 529 ± 84, with a mean conserved segment length of 2.8 cM. This length is <40% of that currently accepted for human and mouse genomes. This means that the mouse and human genomes have diverged at a rate of ∼1.15 rearrangements per million years. By contrast, mouse and rat are diverging at a rate of only ∼0.74 rearrangements per million years.


2005 ◽  
Vol 94 (3) ◽  
pp. 723-730 ◽  
Author(s):  
T. Manabe ◽  
K. Tatsumi ◽  
M. Inoue ◽  
H. Matsuyoshi ◽  
M. Makinodan ◽  
...  
Keyword(s):  

Development ◽  
1997 ◽  
Vol 124 (20) ◽  
pp. 4133-4141 ◽  
Author(s):  
H. Kato ◽  
Y. Taniguchi ◽  
H. Kurooka ◽  
S. Minoguchi ◽  
T. Sakai ◽  
...  

Notch is involved in the cell fate determination of many cell lineages. The intracellular region (RAMIC) of Notch1 transactivates genes by interaction with a DNA binding protein RBP-J. We have compared the activities of mouse RAMIC and its derivatives in transactivation and differentiation suppression of myogenic precursor cells. RAMIC comprises two separate domains, IC for transactivation and RAM for RBP-J binding. Although the physical interaction of IC with RBP-J was much weaker than with RAM, transactivation activity of IC was shown to involve RBP-J by using an RBP-J null mutant cell line. IC showed differentiation suppression activity that was generally comparable to its transactivation activity. The RBP-J-VP16 fusion protein, which has strong transactivation activity, also suppressed myogenesis of C2C12. The RAM domain, which has no other activities than binding to RBP-J, synergistically stimulated transactivation activity of IC to the level of RAMIC. The RAM domain was proposed to compete with a putative co-repressor for binding to RBP-J because the RAM domain can also stimulate the activity of RBP-J-VP16. These results taken together, indicate that differentiation suppression of myogenic precursor cells by Notch signalling is due to transactivation of genes carrying RBP-J binding motifs.


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