Faculty Opinions recommendation of Multilineage transcriptional priming and determination of alternate hematopoietic cell fates.

Author(s):  
Cornelis Murre
Cell ◽  
2006 ◽  
Vol 126 (4) ◽  
pp. 755-766 ◽  
Author(s):  
Peter Laslo ◽  
Chauncey J. Spooner ◽  
Aryeh Warmflash ◽  
David W. Lancki ◽  
Hyun-Jun Lee ◽  
...  

Development ◽  
1996 ◽  
Vol 122 (11) ◽  
pp. 3355-3362 ◽  
Author(s):  
L. Gabay ◽  
H. Scholz ◽  
M. Golembo ◽  
A. Klaes ◽  
B.Z. Shilo ◽  
...  

The induction of different cell fates along the dorsoventral axis of the Drosophila embryo requires a graded activity of the EGF receptor tyrosine kinase (DER). Here we have identified primary and secondary target genes of DER, which mediate the determination of discrete ventral cell fates. High levels of DER activation in the ventralmost cells trigger expression of the transcription factors encoded by ventral nervous system defective (vnd) and pointed P1 (pntPl). Concomitant with the induction of pntP1, high levels of DER activity lead to inactivation of the Yan protein, a transcriptional repressor of Pointed-target genes. These two antagonizing transcription factors subsequently control the expression of secondary target genes such as otd, argos and tartan. The simultaneous effects of the DER pathway on pntP1 induction and Yan inactivation may contribute to the definition of the border of the ventralmost cell fates.


Development ◽  
1992 ◽  
Vol 116 (Supplement) ◽  
pp. 43-51 ◽  
Author(s):  
Charles A. Ettensohn

Cell interactions during gastrulation play a key role in the determination of mesodermal cell fates in the sea urchin embryo. An interaction between primary and secondary mesenchyme cells (PMCs and SMCs, respectively), the two principal populations of mesodermal cells, regulates the expression of SMC fates. PMCs are committed early in cleavage to express a skeletogenic phenotype. During gastrulation, they transmit a signal that suppresses the skeletogenic potential of a subpopulation of SMCs and directs these cells into an alternative developmental pathway. This review summarizes present information concerning the cellular basis of the PMC-SMC interaction, as analyzed by cell transplantation and ablation experiments, fluorescent cell labeling methods and the use of cell type-specific molecular markers. The nature and stability of SMC fate switching, the timing of the PMC-SMC interaction and its quantitative characteristics, and the lineage, numbers and normal fate of the population of skeletogenic SMCs are discussed. Evidence is presented indicating that PMCs and SMCs come into direct filopodial contact during the late gastrula stage, when the signal is transmitted. Finally, evolutionary questions raised by these studies are briefly addressed.


Development ◽  
1998 ◽  
Vol 125 (2) ◽  
pp. 191-200 ◽  
Author(s):  
A. Sapir ◽  
R. Schweitzer ◽  
B.Z. Shilo

Previous work has demonstrated a role for the Drosophila EGF receptor (Torpedo/DER) and its ligand, Gurken, in the determination of anterioposterior and dorsoventral axes of the follicle cells and oocyte. The roles of DER in establishing the polarity of the follicle cells were examined further, by following the expression of DER-target genes. One class of genes (e.g. kekon) is induced by the DER pathway at all stages. Broad expression of kekon at the stage in which the follicle cells migrate posteriorly over the oocyte, demonstrates the capacity of the pathway to pattern all follicle cells except the ventral-most rows. This may provide the spatial coordinates for the ventral-most follicle cell fates. A second group of target genes (e.g. rhomboid (rho)) is induced only at later stages of oogenesis, and may require additional inputs by signals emanating from the anterior, stretch follicle cells. The function of Rho was analyzed by ectopic expression in the stretch follicle cells, and shown to induce a non-autonomous dorsalizing activity that is independent of Gurken. Rho thus appears to be involved in processing a DER ligand in the follicle cells, to pattern the egg chamber and allow persistent activation of the DER pathway during formation of the dorsal appendages.


Immunity ◽  
2006 ◽  
Vol 24 (6) ◽  
pp. 667-669 ◽  
Author(s):  
T. Matt Holl ◽  
Garnett Kelsoe

Development ◽  
2002 ◽  
Vol 129 (7) ◽  
pp. 1763-1774 ◽  
Author(s):  
Scott Cameron ◽  
Scott G. Clark ◽  
Joan B. McDermott ◽  
Eric Aamodt ◽  
H. Robert Horvitz

During Caenorhabditis elegans development, the patterns of cell divisions, cell fates and programmed cell deaths are reproducible from animal to animal. In a search for mutants with abnormal patterns of programmed cell deaths in the ventral nerve cord, we identified mutations in the gene pag-3, which encodes a zinc-finger transcription factor similar to the mammalian Gfi-1 and Drosophila Senseless proteins. In pag-3 mutants, specific neuroblasts express the pattern of divisions normally associated with their mother cells, producing with each reiteration an abnormal anterior daughter neuroblast and an extra posterior daughter cell that either terminally differentiates or undergoes programmed cell death, which accounts for the extra cell corpses seen in pag-3 mutants. In addition, some neurons do not adopt their normal fates in pag-3 mutants. The phenotype of pag-3 mutants and the expression pattern of the PAG-3 protein suggest that in some lineages pag-3 couples the determination of neuroblast cell fate to subsequent neuronal differentiation. We propose that pag-3 counterparts in other organisms determine blast cell identity and for this reason may lead to cell lineage defects and cell proliferation when mutated.


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