The effect of ABA on root growth, secondary-root formation and root gravitropism in seedlings of Zea mays was investigated by using Fluridone-treated seedlings and a viviparous mutant, both of which lack carotenoids and ABA. Primary roots of seedlings grown in the presence of Fluridone grew significantly slower than those of control (i.e. untreated) roots. Elongation of Fluridone-treated roots was inhibited significantly by the exogenous application of 1 mM ABA. Exogenous application of 1 micromole and 1 nmole ABA had either no effect or only a slight stimulatory effect on root elongation, depending on the method of application. The absence of ABA in Fluridone-treated plants was not an important factor in secondary-root formation in seedlings less than 9-10 d old. However, ABA may suppress secondary-root formation in older seedlings, since 11-d-old control seedlings had significantly fewer secondary roots than Fluridone-treated seedlings. Roots of Fluridone-treated and control seedlings were graviresponsive. Similar data were obtained for vp-9 mutants of Z. mays, which are phenotypically identical to Fluridone-treated seedlings. These results indicate that ABA is necessary for neither secondary-root formation nor for positive gravitropism by primary roots.
The molecular determinants governing tissue-specific gene expression in the placenta are at present only poorly defined, particularly with respect to the regulation of specific hormone genes whose products are vital to embryonic development and the maintenance of a nurturing maternal environment. In continuing our analysis of the trophoblast-specific expression of the mouse placental lactogen I gene, we now demonstrate that the transcription factors GATA-2 and GATA-3 regulate the activity of this gene promoter. These factors are expressed in placental trophoblast cells, with peak levels of the GATA-2, GATA-3 and placental lactogen I mRNAs each accumulating at midgestation. Analysis of a region of the placental lactogen I gene promoter, previously shown to be sufficient for directing trophoblast-specific transcription, revealed the presence of three consensus binding sites for GATA-2 or GATA-3. Both GATA-2 and GATA-3 bind to these sites in vitro and mutation of these sites results in a significant decrease in promoter activity as assayed by transient transfection into the choriocarcinoma-derived cell line Rcho-1, which expresses endogenous GATA-2 and GATA-3. Furthermore, overexpression of GATA factors in Rcho-1 cells stimulates transcription from a co-transfected placental lactogen I gene promoter. Most significantly, expression of GATA-2 or GATA-3 was found to induce transcription from this promoter in transfected non-trophoblast (fibroblast) cells. These data indicate that GATA factors are both limiting and required transcriptional regulatory molecules in placental trophoblasts, and that the tissue specificity of the placental lactogen I gene is determined, at least in part, by GATA-2 and/or GATA-3.
We have isolated the gene encoding mouse placental lactogen-I and characterized the promoter region of this gene by transient and stable transfection. Promoter sequences extending 274 basepairs (bp) upstream from the start site of transcription contain all of the elements necessary for maximal expression upon transient transfection into the rat choriocarcinoma Rcho-1 cell line; these Rcho-1 cultures contain both proliferative trophoblast stem cells and terminally differentiated trophoblast giant cells. In stably transfected cell lines, expression from this promoter increases as the percentage of differentiated cells in the culture increases. In contrast to these results in trophoblast cells, the 274-bp promoter as well as a promoter region extending 2700 bp upstream of the transcriptional start site are unable to drive transcription in a variety of other cell types. Mutational and protein binding analyses indicate that two AP-1 sites are required for maximal expression in Rcho-1 cells, and that the composition of the AP-1 transcription factor may vary as differentiation in the cell culture increases.
Chimeric drift is the shift in the proportion over time of the two cell lineages which comprise a chimera (genetic mosaic). Chimeric drift in blood cell populations is determined by both the probability of proliferation from stem cell pools of one or the other of the cell lineages which constitute the chimera and the effects of life span in circulating blood cells. Previous evidence suggests that while chimeric drift occurs in chimeras between genetically disparate strains, it does not occur when the strains used are closely related. No information is available from chimeras between congenic strains. In the present study, chimeric rats were produced between strains with distinguishable class I major histocompatibility complex haplotypes, PVG-RT1a and PVG (which express the haplotype RT1C). PVG-RT 1a-specific monoclonal antibodies were used to establish the mosaic patterns in the cell populations of peripheral blood by fluorescein-activated cell sorting. Mosaic cell lineage of red blood cells, white blood cells, lymphocytes, monocytes and neutrophil populations were analyzed weekly over a period of 6 weeks. The ratio of cells of the PVG-RT la lineage to cells of the PVG lineage shifted either in favor of PVG-RT 1a or PVG in cellular components of peripheral blood. The percentage of PVG-RT1a cells in peripheral blood of chimeras changes by as much as 54, 28, 21, 19 and 23% in red blood cell, white blood cell, lymphocyte, monocyte and neutrophil populations, respectively. The shifts in the percentage of PVG-RT 1a cells appears to occur in a cyclic fashion. Uneven representation and distribution of the two different lineages in stem cell populations has been suggested as a possible mechanism of chimeric drift.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.