Morphological analysis of female gametophyte development in the bel1 stk shp1 shp2 mutant

Abstract

In Arabidopsis thaliana, cell fate in developing ovules is determined by the action of the homeodomain factor BELL1 (BEL1) and of the MADS-box factors SEEDSTICK (STK), SHATTERPROOF1 (SHP1) and SHP2. The analysis of the bel1 and the stk shp1 shp2 mutants revealed that the functional megaspore is formed, however, it does not proceed into megagametogenesis. In the bel1 stk shp1 shp2, quadruple mutant megasporogenesis does not take place. In this article we describe a detailed morphological analysis of the quadruple mutant, and we discuss the possibility that BELL1, STK, SHP1 and SHP2 not only control integument identity determination and development, but that they might also play a role during megasporogenesis.     

TRIM32/USP11 Balances ARID1A Stability and the Oncogenic/Tumor-Suppressive Status of Squamous Cell Carcinoma

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Free Radicals and Carcinogenesis

The role of free radicals and active states of oxygen in human cancer is as yet unresolved. Various lines of evidence provide strong but inferential evidence that free radical reactions can be of crucial importance in certain carcinogenic mechanisms. A central point in considering free radical reactions in carcinogenesis is that human cancer is really a group of highly diverse diseases for which the initial causation and the progression to clinical disease occur through a wide variety of mechanisms. Furthermore, for many human cancers it appears that there are alternate pathways capable of tumor initiation and tumor progression. While for certain of these pathways free radical reactions appear necessary, it is unlikely that there are human cancers for which free radicals, or any other mechanism, are sufficient for the entire processbeginning with the genetic alteration leading to a somatic mutation and eventually resulting in clinically overt disease. It is crucial that we view free radical reactions as aong a panoply of mechanisms leading to human cancer, and consider research about the role of free radicals in cancer as opportunities to prevent the initiation or progression of human cancer.     

The Mitochondrial Protein MAVS Stabilizes p53 to Suppress Tumorigenesis

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Reversible hyperphosphorylation and reorganization of vimentin intermediate filaments by okadaic acid in 9L rat brain tumor cells.

Okadaic acid (OA), a protein phosphatase inhibitor, was found to induce hyperphosphorylation and reorganization of vimentin intermediate filaments in 9L rat brain tumor cells. The process was dose dependent. Vimentin phosphorylation was initially enhanced by 400 nM OA in 30 min and reached maximal level (about 26-fold) when cells were treated with 400 nM OA for 90 min. Upon removal of OA, dephosphorylation of the hyperphosphorylated vimentin was observed and the levels of phosphorylation returned to that of the controls after the cells recovered under normal growing conditions for 11 h. The phosphorylation and dephosphorylation of vimentin induced by OA concomitantly resulted in reversible reorganization of vimentin filaments and alteration of cell morphology. Cells rounded up as they were entering mitosis in the presence of OA and returned to normal appearance after 11 h of recovery. Immuno-staining with anti-vimentin antibody revealed that vimentin filaments were disassembled and clustered around the nucleus when the cells were treated with OA but subsequently returned to the filamentous states when OA was removed. Two-dimensional electrophoresis analysis further revealed that hyperphosphorylation of vimentin generated at least seven isoforms having different isoelectric points. Furthermore, the enhanced vimentin phosphorylation was accompanied by changes in the detergent-solubility of the protein. In untreated cells, the detergent-soluble and -insoluble vimentins were of equal amounts but the solubility could be increased when vimentins were hyperphosphorylated in the presence of OA. Taken together, the results indicated that OA could be involved in reversible hyperphosphorylation and reorganization of vimentin intermediate filaments, which may play an important role in the structure-function regulation of cytoskeleton in the cell.     

Collagen gene construction and evolution

Summary Collagen genes appear to have been assembled by the tandem repetition of homologous primary (9 base pair), secondary (54 base pair), and tertiary (702 base pair) modules. In vertebrate interstitial collagen genes many of the secondary modules are separated by introns, but in invertebrate collagen genes the non-coding sequences lie near the ends of supposed tertiary modules and are therefore about 702 (54×13) base pairs apart. The genes for vertebrate interstitial collagens (types I–III) seem to have been constructed by the tandem repetition of five tertiary modules, three of which were subsequently shortened by internal deletions. This shortening of the gene resulted in the non-integral relationship between the period of the fibrils and the length of the molecules of vertebrate collagens, and was therefore responsible for the mechanical properties of the completed product. Comparisons of the amino acid sequences of various collagens indicate that the main types of collagen evolved about 800–900 million years ago, a date that agrees well with the fossil record of primitive Metazoa.     

Single-cell landscape of the ecosystem in early-relapse hepatocellular carcinoma

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EXO5-DNA structure and BLM interactions direct DNA resection critical for ATR-dependent replication restart

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Glioma-Derived miRNA-Containing Extracellular Vesicles Induce Angiogenesis by Reprogramming Brain Endothelial Cells

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