Faculty Opinions recommendation of Transcription through intergenic chromosomal memory elements of the Drosophila bithorax complex correlates with an epigenetic switch.

Author(s):  
Rob White
Genetics ◽  
1997 ◽  
Vol 145 (1) ◽  
pp. 123-137 ◽  
Author(s):  
Fernando Casares ◽  
Welcome Bender ◽  
John Merriam ◽  
Ernesto Sánchez-Herrero

The Ultrabithorax (Ubx) gene of the Drosophila bithorax complex is required to specify parasegments 5 and 6. Two P-element “enhancer traps” have been recovered within the locus that contain the bacterial lacZ gene under the control of the P-element promoter. The P insertion that is closer to the Ubx promoter expresses lucZ in a pattern similar to that of the normal Ubx gene, but also in parasegment 4 during embryonic development. Two deletions have been recovered that remove the normal Ubx promoter plus several kilobases on either side, but retain the lacZ reporter gene. The lacZ patterns from the deletion derivatives closely match the normal pattern of Ubx expression in late embryos and imaginal discs. The lacZ genes in the deletion derivatives are also negatively regulated by Ubx and activated in trans by Contrabithorax mutations, again like the normal Ubx gene. Thus, the deleted regions, including several kilobases around the Ubx promoter, are not required for long range interactions with Ubx regulatory regions. The deletion derivatives also stimulate transvection, a pairing-dependent interaction with the Ubx promoter on the homologous chromosome.


2021 ◽  
pp. 1-12
Author(s):  
Isatou Bah ◽  
Tuqa Alkhateeb ◽  
Dima Youssef ◽  
Zhi Q. Yao ◽  
Charles E. McCall ◽  
...  

Sepsis-induced myeloid-derived suppressor cells (MDSCs) increase mortality risk. We previously identified that long non-coding RNA Hotairm1 supports myeloid precursor shifts to Gr1<sup>+</sup>CD11b<sup>+</sup> MDSCs during mouse sepsis. A major unanswered question is what molecular processes control Hotairm1 expression. In this study, we found by a genetic deletion that a specific PU.1-binding site is indispensable in controlling Hotairm1 transcription. We then identified H3K4me3 and H3K27me3 at the PU.1 site on the Hotairm1 promoter. Controlling an epigenetic switch of Hotairm1 transcription by PU.1 was histone KDM6A demethylase for H3K27me3 that derepressed its transcription with possible contributions from Ezh2 methyltransferase for H3K27me3. KDM6A knockdown in MDSCs increased H3K27me3, decreased H3K4me3, and inhibited Hotairm1 transcription activation by PU.1. These results enlighten clinical translation research of PU.1 epigenetic regulation as a potential sepsis immune-checkpoint treatment site.


Cell ◽  
2012 ◽  
Vol 149 (4) ◽  
pp. 819-831 ◽  
Author(s):  
Daphne S. Cabianca ◽  
Valentina Casa ◽  
Beatrice Bodega ◽  
Alexandros Xynos ◽  
Enrico Ginelli ◽  
...  

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