Home
Reference Report
| Reference | |||
|---|---|---|---|
| Citation | Shevelyov, Y.Y., Lavrov, S.A., Mikhaylova, L.M., Nurminsky, I.D., Kulathinal, R.J., Egorova, K.S., Rozovsky, Y.M., Nurminsky, D.I. (2009). The B-type lamin is required for somatic repression of testis-specific gene clusters. Proc. Natl. Acad. Sci. U.S.A. 106(9): 3282--3287. (Export to RIS) | ||
| FlyBase ID | FBrf0207453 | ||
| Publication Type | Research paper | ||
| PubMed ID | 19218438 | ||
| PubMed Abstract | Large clusters of coexpressed tissue-specific genes are abundant on chromosomes of diverse species. The genes coordinately misexpressed in diverse diseases are also found in similar clusters, suggesting that evolutionarily conserved mechanisms regulate expression of large multigenic regions both in normal development and in its pathological disruptions. Studies on individual loci suggest that silent clusters of coregulated genes are embedded in repressed chromatin domains, often localized to the nuclear periphery. To test this model at the genome-wide scale, we studied transcriptional regulation of large testis-specific gene clusters in somatic tissues of Drosophila. These gene clusters showed a drastic paucity of known expressed transgene insertions, indicating that they indeed are embedded in repressed chromatin. Bioinformatics analysis suggested the major role for the B-type lamin, LamDm(o), in repression of large testis-specific gene clusters, showing that in somatic cells as many as three-quarters of these clusters interact with LamDm(o). Ablation of LamDm(o) by using mutants and RNAi led to detachment of testis-specific clusters from nuclear envelope and to their selective transcriptional up-regulation in somatic cells, thus providing the first direct evidence for involvement of the B-type lamin in tissue-specific gene repression. Finally, we found that transcriptional activation of the lamina-bound testis-specific gene cluster in male germ line is coupled with its translocation away from the nuclear envelope. Our studies, which directly link nuclear architecture with coordinated regulation of tissue-specific genes, advance understanding of the mechanisms underlying both normal cell differentiation and developmental disorders caused by lesions in the B-type lamins and interacting proteins. | ||
| DOI | 10.1073/pnas.0811933106 | ||
| Related Publication(s) | |||
Recent Updates
|
|||
| Description |
What does this section display?
This section contains items that were added to this record for each release.
It currently only tracks new links between this FlyBase report and other
FlyBase data classes (e.g. genes, references, stocks) or controlled
vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
|
||
| Update Feed |
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your
feed reader.
|
||
| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
|
Associated Information
|
|||
| Comments | |||
| Associated Files | |||
|
Other Information
|
|||
| Secondary IDs | |||
| Language of Publication | English | ||
| Additional Languages of Abstract | |||
| Also Published As | |||
|
Parent Publication
|
|||
| Publication Type | Journal | ||
| Abbreviation | Proc. Natl. Acad. Sci. U.S.A. | ||
| Title | Proceedings of the National Academy of Sciences of the United States of America | ||
| Publication Year | 1915- | ||
| ISBN/ISSN | 0027-8424 | ||
|
Data from Reference
|
|||
| Genes (45)
|
|||