Chromatin Structural Changes in the Putative Regulatory Region of c-myc Accompany the Translocation in a Burkitt Lymphoma

Author(s):  
U. Siebenlist ◽  
L. Hennighausen ◽  
J. Battey ◽  
P. Leder
Cell ◽  
1984 ◽  
Vol 37 (2) ◽  
pp. 381-391 ◽  
Author(s):  
Ulrich Siebenlist ◽  
Lothar Hennighausen ◽  
Jim Battey ◽  
Philip Leder

1986 ◽  
Vol 235 (2) ◽  
pp. 435-439 ◽  
Author(s):  
K M Fukasawa ◽  
S S L Li

The nucleotide sequence of approx. 3 kilobases including the regulatory region, a non-coding exon and the first protein-coding exon from mouse lactate dehydrogenase-A (LDH-A) gene has been determined. The putative initiation sites of transcription and translation were deduced by comparing the nucleotide sequence of mouse LDH-A gene with those of a mouse LDH-A processed pseudogene and the LDH-A full-length cDNAs from rat and human. The tentative TATA and CAAT boxes, and the hexanucleotides CCGCCC have been identified. The sequence of AAATCTTGCTCAA of mouse LDH-A gene has also been found to show striking homology to the cyclic AMP-responsive sequences of eukaryotic genes regulated by cyclic AMP. It has been reported previously that the protein-coding sequence of mouse LDH-A gene is interrupted by six introns and the 3′ untranslated sequence of 485 nucleotides is not interrupted [Li, Tiano, Fukasawa, Yagi, Shimiza, Sharief, Nakashima & Pan (1985) Eur. J. Biochem. 149, 215-225]. An additional intron of 1653 base-pairs was found in the 5′ untranslated sequence of 101 nucleotides at 24 nucleotides upstream to the translation start site. Thus, mouse LDH-A gene containing seven introns spans approx. 11 kilobases and its length of mature mRNA is 1582 nucleotides, excluding the poly(A) tail.


2011 ◽  
Vol 4 (1) ◽  
Author(s):  
Sakino Takayanagi ◽  
Gakuta Toba ◽  
Masayuki Koganezawa ◽  
Tamas Lukacsovich ◽  
Daisuke Yamamoto

2003 ◽  
Vol 198 (9) ◽  
pp. 1427-1437 ◽  
Author(s):  
Hiroyuki Gonda ◽  
Manabu Sugai ◽  
Yukiko Nambu ◽  
Tomoya Katakai ◽  
Yasutoshi Agata ◽  
...  

Pax5 activity is enhanced in activated B cells and is essential for class switch recombination (CSR). We show that inhibitor of differentiation (Id)2 suppresses CSR by repressing the gene expression of activation-induced cytidine deaminase (AID), which has been shown to be indispensable for CSR. Furthermore, a putative regulatory region of AID contains E2A- and Pax5-binding sites, and the latter site is indispensable for AID gene expression. Moreover, the DNA-binding activity of Pax5 is decreased in Id2-overexpressing B cells and enhanced in Id2−/− B cells. The kinetics of Pax5, but not E2A, occupancy to AID locus is the same as AID expression in primary B cells. Finally, enforced expression of Pax5 induces AID transcription in pro–B cell lines. Our results provide evidence that the balance between Pax5 and Id2 activities has a key role in AID gene expression.


1994 ◽  
Vol 14 (8) ◽  
pp. 5318-5325 ◽  
Author(s):  
E Chuang ◽  
D Barnard ◽  
L Hettich ◽  
X F Zhang ◽  
J Avruch ◽  
...  

Genetic and biochemical evidence suggests that the Ras protooncogene product regulates the activation of the Raf kinase pathway, leading to the proposal that Raf is a direct mitogenic effector of activated Ras. Here we report the use of a novel competition assay to measure in vitro the relative affinity of the c-Raf-1 regulatory region for Ras-GTP, Ras-GDP, and 10 oncogenic and effector mutant Ras proteins. c-Raf-1 associates with normal Ras and the oncogenic V12 and L61 forms of Ras with equal affinity. The moderately transforming mutant Ras[E30K31] also bound to the c-Raf-1 regulatory region with normal affinity. Transformation-defective Ras effector mutants Ras[N33], Ras[S35], and Ras[N38] bound poorly. In contrast, the transformation defective Ras[G26I27] and Ras[E45] mutants bound to the c-Raf-1 regulatory region with nearly wild-type affinity. A stable, high-affinity Ras-binding region of c-Raf-1 was mapped to a 99-amino-acid subfragment of the first 257 residues. The smallest Ras-binding region identified consisted of N-terminal residues 51 to 131, although stable expression of the domain and high-affinity binding were improved by the presence of residues 132 to 149. Deletion of the Raf zinc finger region did not reduce Ras-binding affinity, while removal of the first 50 amino acids greatly increased affinity. Phosphorylation of Raf[1-149] by protein kinase A on serine 43 resulted in significant inhibiton of Ras binding. demonstrating that the mechanism of cyclic AMP downregulation results through structural changes occurring exclusively in this small Ras-binding domain.


2017 ◽  
Vol 292 (16) ◽  
pp. 6542-6554 ◽  
Author(s):  
Mithu Guha ◽  
Mario Saare ◽  
Julia Maslovskaja ◽  
Kai Kisand ◽  
Ingrid Liiv ◽  
...  

2018 ◽  
Author(s):  
Kang-Wook Kim ◽  
Benjamin C. Jackson ◽  
Hanyuan Zhang ◽  
David P. L. Toews ◽  
Scott A. Taylor ◽  
...  

AbstractColour polymorphisms play a key role in sexual selection and speciation, yet the mechanisms that generate and maintain them are not fully understood. Here, we use genomic and transcriptomic tools to identify the precise genetic architecture and evolutionary history of a sex-linked colour polymorphism in the Gouldian finch Erythrura gouldiae that is also accompanied by remarkable differences in behaviour and physiology. We find that differences in colour are associated with an ~72-kbp region of the Z chromosome in a putative regulatory region for follistatin, an antagonist of the TGF-β superfamily genes. The region is highly differentiated between morphs, unlike the rest of the genome, yet we find no evidence that an inversion is involved in maintaining the distinct haplotypes. Coalescent simulations confirm that there is elevated nucleotide diversity and an excess of intermediate frequency alleles at this locus. We conclude that this pleiotropic colour polymorphism is most probably maintained by balancing selection.


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