An intronic sequence mutated in flexed-tail mice regulates splicing of Smad5

2007 ◽  
Vol 18 (12) ◽  
pp. 852-860 ◽  
Author(s):  
Shailaja Hegde ◽  
Laurie E. Lenox ◽  
Andrew Lariviere ◽  
Prashanth Porayette ◽  
John M. Perry ◽  
...  
Keyword(s):  
Intronic Sequence ◽  
Flexed Tail

Improving human interferon-β production in mammalian cell lines by insertion of an intronic sequence within its naturally uninterrupted gene

2009 ◽  
Vol 52 (3) ◽  
pp. 191 ◽  
Author(s):  
Paola Zago ◽  
Marco Baralle ◽  
Youhna M. Ayala ◽  
Natasa Skoko ◽  
Serena Zacchigna ◽  
...  
Keyword(s):  
Cell Lines ◽  
Mammalian Cell ◽  
Human Interferon ◽  
Interferon Β ◽  
Intronic Sequence ◽  
Mammalian Cell Lines

scholarly journals Lariat intronic RNAs in the cytoplasm of vertebrate cells

2018 ◽  
Vol 115 (34) ◽  
pp. E7970-E7977 ◽  
Author(s):  
Gaëlle J. S. Talhouarne ◽  
Joseph G. Gall
Keyword(s):  
Cell Lines ◽  
Human Cell ◽  
Biological Significance ◽  
Housekeeping Genes ◽  
Passive Diffusion ◽  
Human Cell Lines ◽  
Intronic Sequence

Most intronic RNAs are degraded within seconds or minutes after their excision from newly formed transcripts. However, stable intronic sequence RNAs (sisRNAs) have been described from oocytes of the frog Xenopus, from Drosophila embryos, and from human cell lines. In Xenopus oocytes, sisRNAs are abundant in both the nucleus and cytoplasm, they occur in the form of lariats, and they are stable for days. In this study we demonstrate that cytoplasmic sisRNAs are also found in human, mouse, chicken, and zebrafish cells. They exist as circular (lariat) molecules, mostly 100–500 nucleotides in length, and are derived from many housekeeping genes. They tend to have an unusual cytosine branchpoint (with the exception of those from the frog). Stable lariats are exported from the nucleus to the cytoplasm by the NXF1/NXT1 system, demonstrating that their presence in the cytoplasm is not due to passive diffusion. Lariats in the cytoplasm are not associated with transcripts of the genes from which they are derived. The biological significance of cytoplasmic sisRNAs remains obscure.

Stable intronic sequence RNAs have possible regulatory roles in Drosophila melanogaster

2015 ◽  
Vol 212 (12) ◽  
pp. 21212OIA99
Author(s):  
Jun Wei Pek ◽  
Ismail Osman ◽  
Mandy Li-Ian Tay ◽  
Ruther Teo Zheng
Keyword(s):  
Drosophila Melanogaster ◽  
Intronic Sequence

scholarly journals Novel BCR-ABL transcript containing an intronic sequence insert in a patient with Philadelphia-positive acute lymphoblastic leukaemia

2000 ◽  
Vol 110 (4) ◽  
pp. 867-870 ◽  
Author(s):  
Masako Hirota ◽  
Eiko Hidaka ◽  
Ichiro Ueno ◽  
Masayo Ishikawa ◽  
Naoko Asano ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukaemia ◽  
Lymphoblastic Leukaemia ◽  
Intronic Sequence

scholarly journals Is RNA editing implicated in group II intron survival in the angiosperm mitochondrial genome?

Genome ◽  
2012 ◽  
Vol 55 (1) ◽  
pp. 75-79 ◽  
Author(s):  
Hiroyo Kagami ◽  
Hironori Nagano ◽  
Yoshiya Takahashi ◽  
Tetsuo Mikami ◽  
Tomohiko Kubo
Keyword(s):  
Sugar Beet ◽  
Rna Editing ◽  
Group Ii Intron ◽  
Intron Loss ◽  
The Other ◽  
Mitochondrial Genomes ◽  
Intronic Sequence ◽  
Sister Clade ◽  
Portulaca Grandiflora ◽  
Group Ii

Introns may be considered as optional because they are removed from mRNA molecules, but introns are fairly preserved for unknown reasons. Previously, the mitochondrial rps3 gene of sugar beet ( Beta vulgaris L., Caryophyllales) was shown to represent a unique example of an intron loss. We have determined the distribution of the rps3 intron in 19 Caryophyllalean species. The intron was absent from the Amaranthaceae and the Achatocarpaceae. In the Caryophyllaceae, Dianthus japonicus rps3 was pseudogenized, but the intronic sequence was retained. Intact intron-bearing rps3 copies were cloned from Portulaca grandiflora and Myrtillocactus geometrizans , members of the sister clade of the Amaranthaceae–Achatocarpaceae–Caryophyllaceae clade. Most of the C-to-U RNA-editing sites in P. grandiflora and M. geometrizans rps3 transcripts were homologous in the two species, as well as in the sugar beet rps3, which, unlike the other 12 rps3 transcripts, lacks editing in the exonic regions around the intron. Provided that the loss of editing preceded the loss of rps3 intron, it appears conceivable that a requirement for editing could have prevented the loss of group II introns retained in angiosperm mitochondrial genomes. This interpretation is an alternative to the conventional one that views the loss of editing as a mere trace of RNA-mediated gene conversion.

BMP4/Madh5 Dependent Signaling Is Required for the Expansion of a Population of Stress Erythroid Progenitors in the Fetal Liver.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4195-4195
Author(s):  
Robert F. Paulson ◽  
Prashanth Porayette
Keyword(s):  
Bone Marrow ◽  
Steady State ◽  
Fetal Liver ◽  
Erythroid Progenitors ◽  
Acute Anemia ◽  
Erythroid Response ◽  
Stress Erythropoiesis ◽  
And Control ◽  
Flexed Tail

Abstract Fetal liver hematopoiesis is primarily erythropoiesis, which robustly produces erythrocytes to meet the growing need of the developing embryo. In many ways fetal liver erythropoiesis resembles stress erythropoiesis in the adult, where in response to acute anemia, a unique population of stress erythroid progenitors is rapidly expanded in the spleen. The development of these stress progenitors requires BMP4/Madh5 dependent signals. Spleen stress progenitors exhibit properties that are distinct from bone marrow steady state progenitors in that they are able to rapidly form large BFU-E colonies, which require only Epo stimulation for their generation. Mice mutant at the flexed-tail locus exhibit a defective stress erythroid response because of a mutation in Madh5. In addition to this defect, flexed-tail mice also exhibit a severe fetal-neonatal anemia. We have analyzed fetal liver erythropoiesis in flexed-tail and control embryos. We show that BMP4 is expressed in the fetal liver and its expression correlates with the time of maximum erythropoiesis. In flexed-tail mutant embryos the expression is delayed and this correlates with both a delay and a defect in the expansion of erythroid progenitors. Our analysis also shows that the fetal liver contains two types of erythroid progenitors. One type exhibits the properties of stress BFU-E found in the adult spleen, which are compromised in flexed-tail embryos and a second type that is similar to bone marrow steady state BFU-E. These data demonstrate that BMP4 dependent signaling drives the expansion of erythroid progenitors in the fetal liver in a manner similar to stress erythropoiesis in the adult spleen.

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