Annual Review of Genetics - Volume 29, 1995

Flower 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.

This 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.

DNA 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.

Upon 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.

Lipid 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.

This 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.

Ustilago 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.