Comment: unresolved questions concerning muscle afferents

Some current questions regarding muscle afferent receptors are discussed. These include the significance of variable distribution patterns of muscle spindles in different muscles and of differences in intrinsic spindle morphology. The significance of the very large and variable population of small myelinated afferent fibres in muscle is also discussed.     

The cytological analysis of causes affecting the root cell length

The final length of the root cell is the result of a series of prooesses which represent a transition of the growing cell from its origin up to the completion of its elongation. These processes are associated on the one hand with cell proliferation, or, after the termination of proliferation, with the proceeding DNA synthesis, and with cell elongation on the other. The group of properties characterizing the growth region of the root as a cytologically heterogeneous complex, is at the same time the group of causes which affect the length of root cells. The individual cases documented in the paper point out the fact that the mechanisms regulating growth processes, have a locally limited action, often only within one single cell, and that they are simultaneously subordinated to the regulatory mechanism which controls the growth of the root as an entirety.     

Cell death in ovarioles causes permanent sterility in Frieseomelitta varia worker bees

Frieseomelitta varia worker bees do not lay eggs even when living in queenless colonies, a condition that favors ovary development and oviposition in the majority of highly social bees. The permanent sterility of these worker bees was initially attributed to a failure in ovary morphogenesis and differentiation. Using transmission electron microscopy we found that at the beginning of the pupal phase the ovaries of F. varia workers are formed by four ovarioles, each of them composed of 1) a terminal filament at the apex of the ovarioles, containing juxtaposed and irregularly shaped cells, 2) a germarium with clusters of cystocytes and prefollicular cells showing long cytoplasmic projections that envelop the cystocyte clusters, 3) fusiform interfollicular and basal stalk precursor cells, and 4) globular, irregularly contoured basal cells with large nuclei. However, during the pupal phase an accentuated and progressive process of cell death takes place in the ovarioles. The dying cells are characterized by large membrane bodies, electron-dense apoptotic bodies, vacuoles, vesiculation, secondary lysosomes, enlarged rough endoplasmic reticulum cisternae, swollen mitochondria, pycnotic nuclei, masses of chromatin adjacent to the convoluted nuclear envelope, and nucleoli showing signs of fragmentation. Cell death continues in ovarioles even after the emergence of the workers. Once they become nurse bees, the ovaries have become transformed into a cell mass in which structurally organized ovarioles can no longer be identified. In F. varia workers, ovariole cell death most certainly is part of the program of caste differentiation.     

Cell adhesion: old and new questions

Metazoans clearly need cell adhesion to hold themselves together, but adhesion does much more than that. Adhesion receptors make transmembrane connections, linking extracellular matrix and adjacent cells to the intracellular cytoskeleton, and they also serve as signal transducers. In this article, I briefly summarize our present understanding of the molecular basis and biological consequences of cell adhesion and discuss how our current knowledge sheds light on questions of specificity of cell adhesion. I offer some thoughts and speculations about the evolution of cell-adhesion molecules and processes, consider their inter-relationships with other forms of cell–cell communication and discuss unresolved questions ripe for investigation as we enter the postgenomic era.     

Cell adhesion: old and new questions

Metazoans clearly need cell adhesion to hold themselves together, but adhesion does much more than that. Adhesion receptors make transmembrane connections, linking extracellular matrix and adjacent cells to the intracellular cytoskeleton, and they also serve as signal transducers. In this article, I briefly summarize our present understanding of the molecular basis and biological consequences of cell adhesion and discuss how our current knowledge sheds light on questions of specificity of cell adhesion. I offer some thoughts and speculations about the evolution of cell-adhesion molecules and processes, consider their inter-relationships with other forms of cell–cell communication and discuss unresolved questions ripe for investigation as we enter the postgenomic era.     

Cell adhesion: old and new questions

Metazoans clearly need cell adhesion to hold themselves together, but adhesion does much more than that. Adhesion receptors make transmembrane connections, linking extracellular matrix and adjacent cells to the intracellular cytoskeleton, and they also serve as signal transducers. In this article, I briefly summarize our present understanding of the molecular basis and biological consequences of cell adhesion and discuss how our current knowledge sheds light on questions of specificity of cell adhesion. I offer some thoughts and speculations about the evolution of cell-adhesion molecules and processes, consider their inter-relationships with other forms of cell–cell communication and discuss unresolved questions ripe for investigation as we enter the postgenomic era.     

Cell death pathology: perspective for human diseases

Apoptosis, a genetically regulated form of cell death with distinct biochemical and morphological features, plays a relevant physiological and pathological role in the organism, being pivotal in the maintenance of tissue development and homeostasis in the adult as well as in the regulation of immune responses. Deregulation of this process causes several human disorders including cancer, autoimmune and neurodegenerative diseases. Thus, modulation of the apoptotic process and of cell death in general, is a potential therapeutic approach for the treatment of several human pathologies.     

Leading causes of childhood death

The over-all rates of death in childhood decreased five to ten fold during the first half of the century, with the greatest drop occurring in deaths due to infections. The death rate due to accidents has shown a relatively slight decrease; hence, accidents are now the leading cause of childhood death, and in California account for 32 per cent of the deaths in the group 1 to 15 years of age. In California, and among certain insured groups of children, cancer is the leading or second leading cause of death due to disease. There is indication that the incidence of leukemia is increasing in early childhood and in the older age groups.Accidents, the leading cause of childhood death, do not happen; they are caused, and so can be prevented. The medical profession should concern itself much more actively in the field of accident prevention.     

Cell death in bioreactors: a role for apoptosis

The incidence of apoptotic and necrotic cell death was compared in CHO, SF9 insect cells and murine plasmacytoma (J558L) and hybridoma (TB/C3) cells during in vitro cultivation in batch cultures. Acridine orange staining and fluorescence microscopy enabled the visualization of a classic morphological feature of apoptotic cell, the presence of condensed and/or fragmented chromatin. DNA gel electrophoresis was employed to show an additional characteristic of the process, the endonuclease-mediated fragmentation of DNA into multiples of 180 base pairs. The levels of apoptosis at the end of batch cultures of plasmacytoma and hybridoma cell lines were found to be 60% and 90% of total dead cells, respectively. However, employing the above-mentioned techniques, the biochemical and morphological features of apoptosis were not found in CHO and SF9 insect cells. Some factors affecting the induction of apoptosis during the batch culture of the hybridoma and plasmacytoma cell lines were identified. The most effective inducer was found to be glutamine limitation, followed by (in order of importance) serum limitation, glucose limitation, and ammonia toxicity. Blockage of the cell cycle of the plasmacytoma and hybridoma cells using thymidine resulted in the induction of apoptosis. This has important implications for the development of cell culture processes that minimize cell division and thereby increase specific productivity. (c) 1994 John Wiley & Sons, Inc.     

Chemical and cytological changes during the autolysis of yeasts

Summary Cell suspensions ofSacharomyces cerevisiae, Kloeckera apiculata andCandida stellata were autolyzed in phosphate buffer, pH 4.5, for up to 10 days. Cell dry weights decreased by 25–35% after 10 days. Based on initial cell dry weight, the soluble autolysate consisted of: carbohydrate (principally polysaccharide) 3–7%; organic acids 3–6%; protein 12–13%; free amino acids 8–12%; nucleic acid products 3–5%; and lipids 1–12%. The main organic acids in autolysates were propionic, succinic and acetic and the main amino acids were phenylalanine, glutamic acid, leucine, alanine and arginine. Approximately 85–90% of cellular RNA and 25–40% of cellular DNA were degraded during autolysis. Both neutral lipid and phospholipid components were degraded, with neutral lipids but not phospholipids being found in autolysates. Scanning and transmission electron micrographs showed retention of cell wall structure and shape during autolysis, but there was extensive intracellular disorganization withinS. cerevisiae andC. stellata. There were differences in the autolytic behavior ofK. apiculata compared withS. cerevisiae andC. stellata.This paper is dedicated to Professor Herman Jan Phaff in honor of his 50 years of active research which still continues.     

Quantitative studies of cytochemical and cytological changes during cell death in the larval fat body of Drosophila melanogaster

Cytometric analysis of larval fat body cells of normal and mutant genotypes was done to ascertain changes in the average cell size, the distribution of cell sizes, and changes in the amounts of cellular reserves after various incubation times in lytic and permissive environments during the lytic phase of cell death. The average cell size becomes smaller in both environments but less rapidly in the permissive environments. The distribution of cell sizes is strikingly broader in the permissive than the lytic environment. Glycogen, lipid, and protein reserves are lost from the cells during the lytic phase but at different rates. Glycogen and lipid reserves are lost independently of the environment. Regardless of whether the environment was lytic or permissive, glycogen disappeared from the cells completely and extremely rapidly whereas lipid disappeared from the cells at a slower rate. Protein was also lost from the cells but the rate was dependent on the environment. There was a rapid loss of protein in the environment which causes rapid cell death, but a gradual loss of protein in the environment where cell death occurs gradually. The relationship of the decrease in cell size and the loss of reserves to the permissiveness of the environment is discussed.     

Cell death pathology: the war against cancer

Programmed cell death was a fundamental discovery, awarded with the Nobel price in 2002 to Sulston, Brenner and Horvitz [1]. Since then it has been clear that alteration of apoptotic pathways is a common feature of tumors, enabling cancer cells to survive chemotherapeutic interventions. Thus, apoptosis is an attractive target in cancer therapy, with the aim to revert the cancer-related alterations of the cell death machinery. Here, we overview the fundamental apoptotic pathways and summarize the attempts to target apoptosis to restore cell death in cancer cells with a special focus on the p53-family and autophagy.     

Cell death in development: shaping the embryo

Cell death in animals is normally classified as type I (apoptotic), type II (autophagic) or necrotic. Of the biologically controlled types of death, in most embryos apoptosis is the most common, although in metamorphosis and in cells with massive cytoplasm type II is often seen, and intermediate forms are seen. For vertebrate embryos other than mammals, apoptosis is not seen prior to gastrulation but thereafter is used to sculpt the organs of the embryo, while overproduction of cells with subsequent death of excess cells is a common means of generating high specificity with low information cost. In zebrafish at least, the inability of embryos prior to the maternal-zygotic transition to undergo apoptosis appears to derive from the inability of the cells to resist lysis once apoptosis begins, rather than any inhibition of apoptosis. In mammalian embryos, apoptosis is seen during cavitation. Thereafter, as in other embryos, cell death plays a major role in shaping and sculpting the embryo. In those situations that have been carefully studied, cell death is under tight genetic control (including regulation of gene products whose function in cell death is not yet known, such as cdk5), with activation of apoptosis sometimes regulated by local environmental variables.