摘要:

AbstractChromosome transmission inS. cerevisiaerequires the activities of many structural and regulatory proteins required for the replication, repair, recombination and segregation of chromosomal DNA, and co‐ordination of the chromosome cycle with progression through the cell cycle. An important structural domain on each chromosome is the kinetochore (centromere DNA and associated proteins), which provides the site of attachment of chromosomes to the spindle microtubules. Stoleret al.(1)have recently reported the cloning of an essential geneCSE4, mutations in which cause chromosome nondisjunction of a marked chromosome bearing a centromere DNA mutation. Thecse4–1mutation causes cells to arrest in the G2/M phase of the cell cycle with a 2N DNA content in aRAD9checkpoint‐independent manner. The carboxyl terminus of Cse4p and the human centromere‐localized protein CENP‐A have a high degree of homology to the C‐terminal domain of histone H3. Since both CENP‐A and Cse4p also have biochemical properties similar to histones H3 and H4, it is tempting to speculate that these histone H3‐like proteins are components of specialized nucleosomes, a class of which may be unique to

ISSN:0265-9247    

DOI:10.1002/bies.950170802

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractTumor suppressor genes represent a broad class of genes that normally function in the negative regulation of cell proliferation. Loss‐of‐function mutations in these genes lead to unrestrained cell proliferation and tumor formation. A fundamental understanding of how tumor suppressor genes regulate cell proliferation and differentiation should reveal important aspects of signalling pathways and cell cycle control. A recent report describing theDrosophilatumor suppressor genewartshas implications in the study of the human myotonic dystrophy gene(1). These genes encode members of a cyclic AMP‐dependent protein kinase subfamily that includes other plant and animal orthol

ISSN:0265-9247    

DOI:10.1002/bies.950170803

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractUbiquitin is the most phylogenetically conserved protein known. This 8,500 Da polypeptide can be covalently attached to cellular proteins as a posttranslational modification. In most cases, the addition of multiple ubiquitin adducts to a protein targets it for rapid degradation by a multisubunit protease known as the 26S proteasome. While the ubiquitin/26S proteasome pathway is responsible for the degradation of the bulk of cellular proteins during homeostasis, it may also be responsible for the rapid loss of protein during the programmed death of certain cells, such as skeletal muscle during insect metamorphosis. In addition, alterations in the expression and regulation of ubiquitin may play significant roles in pathological disorders. For example, dramatic increases in ubiquitin and ubiquitin‐protein conjugates are observed in a wide variety of neurodegenerative disorders, including Alzheimer's disease. Patients suffering from the autoimmune disease systemic lupus erythematosus generate antibodies reacting with ubiquitin and ubiquitinated histones. At present, it is not known whether these changes in ubiquitin expression and regulation initiate pathological changes in these diseases or if they are altered as a consequence of these disorder

ISSN:0265-9247    

DOI:10.1002/bies.950170804

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractA class of maize mutants, collectively known as disease lesion mimics, display discrete disease‐like symptoms in the absence of pathogens. It is intriguing that a majority of these lesion mimics behave as dominant gain‐of‐function mutations. The production of lesions is strongly influenced by light, temperature, developmental state and genetic background. Presently, the biological significance of this lesion mimicry is not clear, although suggestions have been made that they may represent defects in the plants' recognition of, or response to, pathogens. One feature that is common to all lesion mimics is their association with cell death. In plants, as in animals, a number of developmental and pathological processes exist where controlled cell death, whether programmed or triggered in response to physiological or environmental stimuli, constitutes the normal aspect of life. Might disease lesion mimic mutations represent variants where regulation of desirable cell death has gone awry? In this paper we argue that this might be the case, and further conjecture that these mutants offer a unique opportunity for studying the genetic and cellular mechanisms of cell death in p

ISSN:0265-9247    

DOI:10.1002/bies.950170805

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractEpithelial development dictates the shape of an organism. The metamorphic development of aDrosophilaleg precursor into an adult leg is a well‐defined example of epithelial morphogenesis that can be analyzed from the perspectives of genetics and molecular and cell biology. The steroid hormone 20‐hydroxyecdysone induces and regulates the entire process. Mutants affectingDrosophilaleg morphogenesis characteristically have short thick legs (the malformed phenotype) resulting from a failure to execute normal cell shape changes at a specific stage of development. Mutations that cause the malformed phenotype have already led to the identification and cloning of genes encoding transcription factors, a transmembrane serine protease presumably required for modification of the apical extracellular matrix, and components of the contractile cytoskeleton and adherens junctions. All of these products are required for the execution of normal changes in leg cell sh

ISSN:0265-9247    

DOI:10.1002/bies.950170806

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractPolycystic kidney disease (PKD) is one of the most prevalent causes of heritable renal failure. The disease is characterized by the occurrence of numerous fluid‐filled cysts within the parenchyma of kidney. The cysts are epithelial in origin and expand in size, leading to crowding of normal kidney tissue. Ultimately, there is gross enlargement of the kidneys with loss of normal functions, and death usually occurs because of complications related to renal failure. Animal models of polycystic kidney disease are proving to be extremely useful for studying the molecular basis of renal cyst formation and for the isolation of genes carrying the mutations. This article describes the various animal models of polycystic kidney disease, spontaneously and experimentally derived, that have recently been identifie

ISSN:0265-9247    

DOI:10.1002/bies.950170807

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractThe DNA of all species is constantly under threat from both endogenous and exogenous factors, which damage its chemical structure. Probably the most common lesion that arises in cellular DNA is the loss of a base to generate an abasic site, which is usually referred to as an apurinic or apyrimidinic (AP) site. Since these lesions are potentially both cytotoxic and mutagenic, cells of all organisms express dedicated repair enzymes, termed AP endonucleases, to counteract their damaging effects. Indeed, many organisms consider it necessary to express two or more of these lesion‐specific endonucleases, underscoring the requirement that exists to remove AP sites for the maintenance of genome integrity and cell viability. Most AP endonucleases are very versatile enzymes, capable of performing numerous additional repair roles. In this article, we review the AP endonuclease class of repair enzymes, with emphasis on the evolutionary conservation of structural features, not only between prokaryotic and eukaryotic homologues, but also between these enzymes and the RNase H domain of one class of reverse transcriptas

ISSN:0265-9247    

DOI:10.1002/bies.950170808

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractRecent studies of gene expression in the developing fruitfly leg support a model – Meinhardt's Boundary Model – which seems to contradict the prevailing paradigm for pattern formation in the imaginal discs ofDrosophila– the Polar Coordinate Model. Reasoning from geometric first principles, this article examines the strengths and weaknesses of these hypotheses, plus some baffling phenomena that neither model can comfortably explain. The deeper question at issue is: how does the fly's genome encode the three‐dimensional anatomy of the adult? Does it demarcate territories and boundaries (as in a geopolitical map) and then use those boundaries and their points of intersection as a scaffolding on which to erect the anatomy (the Boundary Model)? Or does it assign cellular fates within a relatively seamless coordinate system (the Polar Coordinate Model)? The existence of hybrid Cartesian‐polar models shows that the alternatives may not be so clear‐cut: a single organ might utilize different systems that are spatially superimposed or temporally

ISSN:0265-9247    

DOI:10.1002/bies.950170809

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractInhibiting the progress of replication forks inE. colimakes them susceptible to breakage. Broken replication forks are evidently reassembled by the RecBCD recombinational repair pathway. These findings explain a particular pattern of DNA degradation during inhibition of chromosomal replication, the role of recombination in the viability of mutants with displaced replication origin, and hyper‐recombination observed in the Terminus of theE. colichromosome inrnhmutants. Breakage and repair of inhibited replication forks could be the reason for the recombination‐dependence of inducible stable DNA replication. A mechanism by which RecABCD‐dependent recombination between very short inverted repeats may helpE. colito invert an operon, transcribed in the direction opposite to that of DNA replication, is disc

ISSN:0265-9247    

DOI:10.1002/bies.950170810

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:0265-9247    

DOI:10.1002/bies.950170811

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY