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- Volume 29, 1995
Annual Review of Genetics - Volume 29, 1995
Volume 29, 1995
- Review Articles
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THE GENETICS OF FLOWER DEVELOPMENT: From Floral Induction to Ovule Morphogenesis
Vol. 29 (1995), pp. 19–39More LessFlower development consists of several phases. The first step is the transition from vegetative to reproductive development, regulated by floral induction. Later steps include the initiation of individual flowers, the determination of organ identity, and organ-specific differentiation. One of the major discoveries of plant biology is that the genetic network controlling flower development is highly conserved in two distantly related dicots, Arabidopsis thaliana and Antirrhinum majus, and probably in other species as well. Classical genetics has identified a sizable number of genes regulating flower development, and many of these regulatory genes have been cloned. This review summarizes recent advances in the understanding of the genetic control of floral induction and determination of flower-meristem identity, with the focus on Arabidopsis thaliana. In addition, recent work on ovule morphogenesis, a late process in flower development, is discussed.
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CHROMOSOME PARTITIONING IN BACTERIA
R. G. Wake, and J. ErringtonVol. 29 (1995), pp. 41–67More LessThis review addresses chromosome partitioning in Escherichia coli and Bacillus subtilis. The first part deals with events associated with completion of a round of replication to an extent that yields separable chromosomes. Events more directly involved in chromosome movement are covered in the second part. In the final section, a model for chromosome partitioning based on the information presented in the first two parts is presented.
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DNA REPAIR IN HUMANS
Vol. 29 (1995), pp. 69–105More LessDNA repair is an important molecular defense system against agents that cause cancer, degenerative diseases, and aging. Several repair systems in humans protect the genome by repairing modified bases, DNA adducts, cross links, and double strand breaks. These repair systems, base excision, nucleotide excision, and recombination, are intimately connected to transcription and to cell cycle checkpoints. In addition, genotoxic stress induces a set of cellular reactions mediated by the p53 tumor suppressor and the Ras oncogene. These genotoxic response reactions may help the cell survive or enter apoptosis. Damage-response reactions may be utilized as targets of anticancer chemotherapy.
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THE PLANT RESPONSE IN PATHOGENESIS, SYMBIOSIS, AND WOUNDING: Variations on a Common Theme?
C. Baron, and P. C. ZambryskiVol. 29 (1995), pp. 107–129More LessUpon interaction with pathogenic Pseudomonads or symbiotic Rhizobia, or after wounding by abrasion or insects, the plant reacts in superficially different ways, leading to either a close association or defense against the intruder. However, a closer examination reveals that similar genes and metabolic pathways are induced. This raises the possibility that signal perception and transduction proceed via similar pathways, leading to overlaps in the response reaction. This review compares current knowledge of the plant reaction to apparently different biotic and abiotic stimuli, and highlights that within the course of evolution similar response mechanisms were adapted to specific needs.
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MEMBRANE PROTEIN ASSEMBLY: GENETIC, EVOLUTIONARY AND MEDICAL PERSPECTIVES
Colin Manoil, and Beth TraxlerVol. 29 (1995), pp. 131–150More LessLipid bilayers are delicate structures that are easily disrupted by a variety of amphipathic molecules. Yet the viability of a cell requires the continued assembly of large amphipathic proteins within its membranes without damage. The need to minimize bilayer disruption may account for a number of fundamental features of membrane protein assembly. These include the use of redundant sequence information to establish the topologies and folded structures of membrane proteins and the existence of efficient mechanisms to rid cells of misassembled proteins. Most missense mutations that inactivate a membrane protein probably do so by altering the folding of the membrane-inserted structure rather than by rearranging the topology or by changing key residues involved directly in function. Such misfolded membrane proteins may be toxic to cells if they escape cellular safeguards. This toxicity may underlie some human degenerative diseases due to mutant membrane proteins.
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MOLECULAR GENETIC ASPECTS OF HUMAN MITOCHONDRIAL DISORDERS
Vol. 29 (1995), pp. 151–178More LessThis review focuses on mutations of mitochondrial DNA (mtDNA) which are an important cause of mitochondrial disorders in humans and are also associated with common neurodegenerative disorders and aging. The high copy number of mtDNA and its maternal transmission make the inheritance of mtDNA mutations fundamentally different from the Mendelian inheritance of nuclear DNA mutations. There is often a mixture of wild-type and mutated mtDNAs (heteroplasmy), and heterogeneity in the distribution of mutated mtDNAs is one plausible explanation for the widely varying phenotypes in patients with mitochondrial disorders. The application of molecular genetics has led to significant progress in the studies of human mitochondrial disorders in the past decade. Future studies including the development of animal models are needed to advance our understanding of the pathogenesis of mitochondrial disorders to enable, in tum, the development of novel therapies and genetic rescue strategies for the treatment of human disease.
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GENETICS OF USTILAGO MAYDIS, A FUNGAL PATHOGEN THAT INDUCES TUMORS IN MAIZE
Vol. 29 (1995), pp. 179–208More LessUstilago maydis induces tumors in maize. It is dimorphic, with a unicellular, nonpathogenic form, and a dikaryotic, filamentous, pathogenic form that requires the plant for its growth. The life cycle is regulated by two mating type loci,a and b: a has two alleles, which encode a pheromone and a receptor; b is multiallelic and encodes a combinatorial homeodomain protein. Cell fusion occurs between haploid cells with different a alleles. The dikaryon formed exhibits filamentous growth if the cells also carry any two different b alleles. The b locus is the major pathogenicity determinant, fuz7, which encodes a MAP kinase activator, is also necessary for tumor induction and may respond to plant signals. Several other genes have been identified (fuz1, fuz2, rtf1, uac, ubc) that affect different aspects of the life cycle transitions. Some of them may identify targets of the b locus. Signaling between pathogen and plant is of key importance in tumor induction and fungal growth and differentiation within the plant. The role of siderophores is also discussed.
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Previous Volumes
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Volume 58 (2024)
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Volume 57 (2023)
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Volume 56 (2022)
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Volume 55 (2021)
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Volume 54 (2020)
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Volume 53 (2019)
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Volume 52 (2018)
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Volume 51 (2017)
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Volume 50 (2016)
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Volume 49 (2015)
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Volume 48 (2014)
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Volume 47 (2013)
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Volume 46 (2012)
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Volume 45 (2011)
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Volume 44 (2010)
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Volume 43 (2009)
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Volume 42 (2008)
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Volume 41 (2007)
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Volume 40 (2006)
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Volume 39 (2005)
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Volume 38 (2004)
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Volume 37 (2003)
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Volume 36 (2002)
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Volume 35 (2001)
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Volume 34 (2000)
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Volume 33 (1999)
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Volume 32 (1998)
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Volume 31 (1997)
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Volume 30 (1996)
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Volume 29 (1995)
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Volume 28 (1994)
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Volume 27 (1993)
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Volume 26 (1992)
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Volume 25 (1991)
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Volume 24 (1990)
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Volume 23 (1989)
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Volume 22 (1988)
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Volume 21 (1987)
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Volume 20 (1986)
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Volume 19 (1985)
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Volume 18 (1984)
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Volume 17 (1983)
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Volume 16 (1982)
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Volume 15 (1981)
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Volume 14 (1980)
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Volume 13 (1979)
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Volume 12 (1978)
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Volume 11 (1977)
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Volume 10 (1976)
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Volume 9 (1975)
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Volume 8 (1974)
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Volume 7 (1973)
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Volume 6 (1972)
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Volume 5 (1971)
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Volume 4 (1970)
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Volume 3 (1969)
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Volume 2 (1968)
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Volume 1 (1967)
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Volume 0 (1932)