Morphological, anatomical, submicroscopical, and physiological changes in whole seeds and embryos of Pisum sativum L. cv. Victory Freezer were followed during 54 days of development of the seed. Four developmental phases-cell formation, cell expansion, synthesis of storage reserves, and maturation and dormancy-were recognized in the development of the embryo. Each phase was characterized by a distinctive physiology and a distinctive subcellular organization of the parenchyma cells. The subcellular organization associated with carbohydrate, protein, and fat metabolism and the significance of membranes in cell organization is described.
Superficial scald in Gl'Rlllly Smith apples has been examined by electron microscopy, and a detailed picture of the changes in cell structure as macroscopic scald symptoms develop has been obtained.
Observations were made by electron microscopy of the leaf cells of normal
(full nutrient) tomato, spinach, and maize plants and of plants grown deficient in
each of the known essential macro- and micronutrients except chlorine. In the
case of spinach, observations were also made by phase contrast and fluorescence
microscopy. A feature of this study was the large variation found in the shape,
size, and appearance of chloroplast sections from both full-nutrient and mineral deficient
plants. A representative range of photographs showing this variation
is presented. Specific changes in chloroplast appearance were found in the cases
of manganese deficiency and iron deficiency and distinctive changes were found
in the 10 other deficiencies. The results obtained are discussed in relation to other
published results describing the effects of mineral deficiencies on plant cell ultrastructure.
ld;&.2qTo gain insight into the regulation of hmi-er1 expression, we cloned a human genomic DNA fragment containing one of the two hmi-er1 promoters and consisting of 1460 bp upstream of the translation initiation codon of hMI-ER1. Computer-assisted sequence analysis revealed that the hmi-er1 promoter region contains a CpG island but lacks an identifiable TATA element, initiator sequence and downstream promoter element. This genomic DNA was able to direct transcription of a luciferase reporter gene in a variety of human cell lines, and the minimal promoter was shown to be located within ؊68/؉144 bp. Several putative Sp1 binding sites were identified, and we show that Sp1 can bind to the hmi-er1 minimal promoter and increase transcription, suggesting that the level of hmi-er1 expression may depend on the availability of Sp1 protein. Functional analysis revealed that hMI-ER1 represses Sp1-activated transcription from the minimal promoter by a histone deacetylase-independent mechanism. Chromatin immunoprecipitation analysis demonstrated that both Sp1 and hMI-ER1 are associated with the chromatin of the hmi-er1 promoter and that overexpression of hMI-ER1 in cell lines that allow Tet-Oninducible expression resulted in loss of detectable Sp1 from the endogenous hmi-er1 promoter. The mechanism by which this occurs does not involve binding of hMI-ER1 to cis-acting elements. Instead, we show that hMI-ER1 physically associates with Sp1 and that endogenous complexes containing the two proteins could be detected in vivo. Furthermore, hMI-ER1 specifically interferes with binding of Sp1 to the hmi-er1 minimal promoter as well as to an Sp1 consensus oligonucleotide. Deletion analysis revealed that this interaction occurs through a region containing the SANT domain of hMI-ER1. Together, these data reveal a functional role for the SANT domain in the action of co-repressor regulatory factors and suggest that the association of hMI-ER1 with Sp1 represents a novel mechanism for the negative regulation of Sp1 target promoters.
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