scholarly journals Lmx1a drives Cux2 expression in the cortical hem through activation of a conserved intronic enhancer

Development ◽  
2019 ◽  
Vol 146 (5) ◽  
pp. dev170068 ◽  
Author(s):  
Santiago P. Fregoso ◽  
Brett E. Dwyer ◽  
Santos J. Franco
Keyword(s):  
Intronic Enhancer ◽  
Cortical Hem

Characterization of an intronic enhancer that regulates myelin proteolipid protein (Plp) gene expression in oligodendrocytes

2005 ◽  
Vol 82 (3) ◽  
pp. 346-356 ◽  
Author(s):  
Fanxue Meng ◽  
Olga Zolova ◽  
Natalia A. Kokorina ◽  
Anna Dobretsova ◽  
Patricia A. Wight
Keyword(s):  
Gene Expression ◽  
Proteolipid Protein ◽  
Myelin Proteolipid Protein ◽  
Intronic Enhancer ◽  
Myelin Proteolipid ◽  
Plp Gene Expression

scholarly journals Critical roles of the immunoglobulin intronic enhancers in maintaining the sequential rearrangement of IgH and Igk loci

2006 ◽  
Vol 203 (7) ◽  
pp. 1721-1732 ◽  
Author(s):  
Matthew A. Inlay ◽  
Tongxiang Lin ◽  
Heather H. Gao ◽  
Yang Xu
Keyword(s):  
B Cells ◽  
Developmental Stage ◽  
Heavy Chain ◽  
Light Chain ◽  
Matrix Attachment Region ◽  
Cis Elements ◽  
Wild Type ◽  
Intronic Enhancer ◽  
Attachment Region

V(D)J recombination of immunoglobulin (Ig) heavy (IgH) and light chain genes occurs sequentially in the pro– and pre–B cells. To identify cis-elements that dictate this order of rearrangement, we replaced the endogenous matrix attachment region/Igk intronic enhancer (MiEκ) with its heavy chain counterpart (Eμ) in mice. This replacement, denoted EμR, substantially increases the accessibility of both Vκ and Jκ loci to V(D)J recombinase in pro–B cells and induces Igk rearrangement in these cells. However, EμR does not support Igk rearrangement in pre–B cells. Similar to that in MiEκ−/− pre–B cells, the accessibility of Vκ segments to V(D)J recombinase is considerably reduced in EμR pre–B cells when compared with wild-type pre–B cells. Therefore, Eμ and MiEκ play developmental stage-specific roles in maintaining the sequential rearrangement of IgH and Igk loci by promoting the accessibility of V, D, and J loci to the V(D)J recombinase.

scholarly journals NF-κB RegulatesBCL3Transcription in T Lymphocytes Through an Intronic Enhancer

2003 ◽  
Vol 171 (8) ◽  
pp. 4210-4218 ◽  
Author(s):  
Baosheng Ge ◽  
Olga Li ◽  
Phillip Wilder ◽  
Angie Rizzino ◽  
Timothy W. McKeithan
Keyword(s):  
T Lymphocytes ◽  
Intronic Enhancer

scholarly journals C/EBP  Regulates Human Adiponectin Gene Transcription Through an Intronic Enhancer

Diabetes ◽  
2005 ◽  
Vol 54 (6) ◽  
pp. 1744-1754 ◽  
Author(s):  
L. Qiao ◽  
P. S. MacLean ◽  
J. Schaack ◽  
D. J. Orlicky ◽  
C. Darimont ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Adiponectin Gene ◽  
Intronic Enhancer

The Foxh1-dependent autoregulatory enhancer controls the level of Nodal signals in the mouse embryo

Development ◽  
2002 ◽  
Vol 129 (14) ◽  
pp. 3455-3468 ◽  
Author(s):  
Dominic P. Norris ◽  
Jane Brennan ◽  
Elizabeth K. Bikoff ◽  
Elizabeth J. Robertson
Keyword(s):  
Mouse Embryo ◽  
Late Onset ◽  
Axis Formation ◽  
Visceral Endoderm ◽  
Mouse Development ◽  
Developmental Abnormalities ◽  
Intronic Enhancer ◽  
Vertebrate Embryo ◽  
Early Mouse ◽  
Pitx2 Expression

The TGFβ-related growth factor Nodal governs anteroposterior (AP) and left-right (LR) axis formation in the vertebrate embryo. A conserved intronic enhancer (ASE), containing binding sites for the fork head transcription factor Foxh1, modulates dynamic patterns of Nodal expression during early mouse development. This enhancer is responsible for early activation of Nodal expression in the epiblast and visceral endoderm, and at later stages governs asymmetric expression during LR axis formation. We demonstrate ASE activity is strictly Foxh1 dependent. Loss of this autoregulatory enhancer eliminates transcription in the visceral endoderm and decreases Nodal expression in the epiblast, but causes surprisingly discrete developmental abnormalities. Thus lowering the level of Nodal signaling in the epiblast disrupts both orientation of the AP axis and specification of the definitive endoderm. Targeted removal of the ASE also dramatically reduces left-sided Nodal expression, but the early events controlling LR axis specification are correctly initiated. However loss of the ASE disrupts Lefty2 (Leftb) expression and causes delayed Pitx2 expression leading to late onset, relatively minor LR patterning defects. The feedback loop is thus essential for maintenance of Nodal signals that selectively regulate target gene expression in a temporally and spatially controlled fashion in the mouse embryo.

scholarly journals The Role of Transcription Factor PU.I in the Activity of the Intronic Enhancer of the Eosinophil-Derived Neurotoxin (RNS2) Gene

Blood ◽  
1998 ◽  
Vol 91 (6) ◽  
pp. 2126-2132 ◽  
Author(s):  
Thamar B. van Dijk ◽  
Eric Caldenhoven ◽  
Jan A.M. Raaijmakers ◽  
Jan-Willem J. Lammers ◽  
Leo Koenderman ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Point Mutations ◽  
Proximal Promoter ◽  
Multiple Forms ◽  
Enhancer Activity ◽  
Promoter Sequences ◽  
Intronic Enhancer ◽  
First Intron ◽  
Shift Analysis

Eosinophil-derived neurotoxin (EDN) found in the granules of human eosinophils is a cationic ribonuclease toxin. Expression of the EDN gene (RNS2) in eosinophils is dependent on proximal promoter sequences in combination with an enhancer located in the first intron. We further define here the active region of the intron using transfections in differentiated eosinophilic HL60 cells. We show that a region containing a tandem PU.I binding site is important for intronic enhancer activity. This region binds multiple forms of transcription factor PU.I as judged by gel-shift analysis and DNA affinity precipitation. Importantly, introducing point mutations in the PU.I site drastically reduces the intronic enhancer activity, showing the importance of PU.I for expression of EDN in cells of the eosinophilic lineage.

Pax6 is required for establishing naso-temporal and dorsal characteristics of the optic vesicle

Development ◽  
2002 ◽  
Vol 129 (19) ◽  
pp. 4535-4545 ◽  
Author(s):  
Nicole Bäumer ◽  
Till Marquardt ◽  
Anastassia Stoykova ◽  
Ruth Ashery-Padan ◽  
Kamal Chowdhury ◽  
...  
Keyword(s):  
Ganglion Cells ◽  
Eye Development ◽  
Genetic Network ◽  
Axis Formation ◽  
Pax6 Gene ◽  
Optic Vesicle ◽  
Intronic Enhancer ◽  
Key Factor ◽  
Lens Formation

The establishment of polarity is an important step during organ development. We assign a function for the paired and homeodomain transcription factor Pax6 in axis formation in the retina. Pax6 is a key factor of the highly conserved genetic network implicated in directing the initial phases of eye development. We recently demonstrated that Pax6 is also essential for later aspects of eye development, such as lens formation and retinogenesis. In this study, we present evidence that a highly conserved intronic enhancer, α, in the Pax6 gene is essential for the establishment of a distalhigh-proximallow gradient of Pax6 activity in the retina. In the mature retina, the activity mediated by the α-enhancer defines a population of retinal ganglion cells that project to two sickle-shaped domains in the superior colliculus and lateral geniculate nucleus. Deletion of the α-enhancer in vivo revealed that retinal Pax6 expression is regulated in two complementary topographic domains. We found that Pax6 activity is required for the establishment, as well as the maintenance of dorsal and nasotemporal characteristics in the optic vesicle and, later, the optic cup.

The hem of the embryonic cerebral cortex is defined by the expression of multiple Wnt genes and is compromised in Gli3-deficient mice

Development ◽  
1998 ◽  
Vol 125 (12) ◽  
pp. 2315-2325 ◽  
Author(s):  
E.A. Grove ◽  
S. Tole ◽  
J. Limon ◽  
L. Yip ◽  
C.W. Ragsdale
Keyword(s):  
Gene Expression ◽  
Cerebral Cortex ◽  
Choroid Plexus ◽  
Gene Families ◽  
Cubitus Interruptus ◽  
Embryonic Mouse ◽  
Developmental Relationship ◽  
Cortical Hem ◽  
Deficient Mice

In the developing vertebrate CNS, members of the Wnt gene family are characteristically expressed at signaling centers that pattern adjacent parts of the neural tube. To identify candidate signaling centers in the telencephalon, we isolated Wnt gene fragments from cDNA derived from embryonic mouse telencephalon. In situ hybridization experiments demonstrate that one of the isolated Wnt genes, Wnt7a, is broadly expressed in the embryonic telencephalon. By contrast, three others, Wnt3a, 5a and a novel mouse Wnt gene, Wnt2b, are expressed only at the medial edge of the telencephalon, defining the hem of the cerebral cortex. The Wnt-rich cortical hem is a transient, neuron-containing, neuroepithelial structure that forms a boundary between the hippocampus and the telencephalic choroid plexus epithelium (CPe) throughout their embryonic development. Indicating a close developmental relationship between the cortical hem and the CPe, Wnt gene expression is upregulated in the cortical hem both before and just as the CPe begins to form, and persists until birth. In addition, although the cortical hem does not show features of differentiated CPe, such as expression of transthyretin mRNA, the CPe and cortical hem are linked by shared expression of members of the Bmp and Msx gene families. In the extra-toesJ (XtJ) mouse mutant, telencephalic CPe fails to develop. We show that Wnt gene expression is deficient at the cortical hem in XtJ/XtJ mice, but that the expression of other telencephalic developmental control genes, including Wnt7a, is maintained. The XtJ mutant carries a deletion in Gli3, a vertebrate homolog of the Drosophila gene cubitus interruptus (ci), which encodes a transcriptional regulator of the Drosophila Wnt gene, wingless. Our observations indicate that Gli3 participates in Wnt gene regulation in the vertebrate telencephalon, and suggest that the loss of telencephalic choroid plexus in XtJ mice is due to defects in the cortical hem that include Wnt gene misregulation.

IgH intronic enhancer

1998 ◽  
pp. 563-564
Author(s):  
Tak W. Mak ◽  
Josef Penninger ◽  
John Roder ◽  
Janet Rossant ◽  
Mary Saunders
Keyword(s):  
Intronic Enhancer
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