Annual Review of Genetics - Volume 42, 2008

Polyploidy is a common mode of evolution in flowering plants. The profound effects of polyploidy on gene expression appear to be caused more by hybridity than by genome doubling. Epigenetic mechanisms underlying genome-wide changes in expression are as yet poorly understood; only methylation has received much study, and its importance varies among polyploids. Genetic diploidization begins with the earliest responses to genome merger and doubling; less is known about chromosomal diploidization. Polyploidy duplicates every gene in the genome, providing the raw material for divergence or partitioning of function in homoeologous copies. Preferential retention or loss of genes occurs in a wide range of taxa, suggesting that there is an underlying set of principles governing the fates of duplicated genes. Further studies are required for general patterns to be elucidated, involving different plant families, kinds of polyploidy, and polyploids of different ages.

Despite recent elucidation of the three-dimensional structure of major photosynthetic complexes, our understanding of light energy conversion in plant chloroplasts and microalgae under physiological conditions requires exploring the dynamics of photosynthesis. The photosynthetic apparatus is a flexible molecular machine that can acclimate to metabolic and light fluctuations in a matter of seconds and minutes. On a longer time scale, changes in environmental cues trigger acclimation responses that elicit intracellular signaling between the nucleo-cytosol and chloroplast resulting in modification of the biogenesis of the photosynthetic machinery. Here we attempt to integrate well-established knowledge on the functional flexibility of light-harvesting and electron transfer processes, which has greatly benefited from genetic approaches, with data derived from the wealth of recent transcriptomic and proteomic studies of acclimation responses in photosynthetic eukaroytes.

Most, if not all, cell types and tissues display several aspects of polarization. In addition to the ubiquitous epithelial cell polarity along the apical-basolateral axis, many epithelial tissues and organs are also polarized within the plane of the epithelium. This is generally referred to as planar cell polarity (PCP; or historically, tissue polarity). Genetic screens in Drosophila pioneered the discovery of core PCP factors, and subsequent work in vertebrates has established that the respective pathways are evolutionarily conserved. PCP is not restricted only to epithelial tissues but is also found in mesenchymal cells, where it can regulate cell migration and cell intercalation. Moreover, particularly in vertebrates, the conserved core PCP signaling factors have recently been found to be associated with the orientation or formation of cilia. This review discusses new developments in the molecular understanding of PCP establishment in Drosophila and vertebrates; these developments are integrated with new evidence that links PCP signaling to human disease.

The staphylococcal agr locus encodes a quorum sensing (QS) system that controls the expression of virulence and other accessory genes by a classical two-component signaling module. Like QS modalities in other Gram-positive bacteria, agr encodes an autoactivating peptide (AIP) that is the inducing ligand for AgrC, the agr signal receptor. Unlike other such systems, agr variants have arisen that show strong cross-inhibition in heterologous combinations, with important evolutionary implications. Also unlike other systems, the effector of global gene regulation in the agr system is a major regulatory RNA, RNAIII. In this review, we describe the functions of the agr system's elements, show how they interact to bring about the regulatory response, and discuss the role of QS in staphylococcal pathobiology. We conclude with the suggestion that agr autoactivation, unlike classical enzyme induction, can occur under suboptimal conditions and can distinguish self from non-self by inducing an exclusive and coordinated population wide response.

Humans, mice, and even kangaroos have an XX female:XY male system of sex determination, in which the Y harbors a male-dominant sex-determining gene SRY. Birds have the opposite, ZZ males and ZW females, and may use a dosage-sensitive Z-borne gene. Other reptiles have genetic sex but no visible sex chromosomes, or determine sex by temperature of egg incubation. How can we make sense of so much variation? How do systems change in evolution? Studies of some unlikely animals—platypus and dragon lizards, frogs and fish—confirm that evolutionary transitions have occurred between TSD and GSD systems, between XY and ZW systems, and even between male and female heterogametic systems. Here I explore nonmodel systems that offer some new perspectives on some venerable questions of sex and sex chromosomes.

Retrotransposons mobilize via RNA intermediates and usually carry with them the agent of their mobility, reverse transcriptase. Retrotransposons are streamlined, and therefore rely on host factors to proliferate. However, retrotransposons are exposed to cellular forces that block their paths. For this review, we have selected for our focus elements from among target-primed (TP) retrotransposons, also called non-LTR retrotransposons, and extrachromosomally-primed (EP) retrotransposons, also called LTR retrotransposons. The TP retrotransposons considered here are group II introns, LINEs and SINEs, whereas the EP elments considered are the Ty and Tf retrotransposons, with a brief comparison to retroviruses. Recurring themes for these elements, in hosts ranging from bacteria to humans, are tie-ins of the retrotransposons to RNA metabolism, DNA replication and repair, and cellular stress. Likewise, there are parallels among host-cell defenses to combat rampant retrotransposon spread. The interactions between the retrotransposon and the host, and their coevolution to balance the tension between retrotransposon proliferation and host survival, form the basis of this review.

Marine eukaryotic photosynthesis is dominated by a diverse group of unicellular organisms collectively called microalgae. Microalgae include cells derived from a primary endosymbiotic event (similar to land plants) and cells derived from subsequent secondary and/or tertiary endosymbiotic events. These latter cells are chimeras of several genomes and dominate primary production in the marine environment. Two consequences of multiple endosymbiotic events include complex targeting mechanisms to allow nuclear-encoded proteins to be imported into the plastid and coordination of enzymes, potentially from disparate originator cells, to form complete metabolic pathways. In this review, we discuss the forces that shaped the genomes of marine microalgae and then discuss some of the metabolic consequences of such a complex evolutionary history. We focus our metabolic discussion on carbon, nitrogen, and iron. We then discuss biomineralization and new evidence for programmed cell death in microalgae. We conclude with a short summary on advances in genetic manipulation of microalgae and thoughts on the future directions of marine algal genomics.

An ATP-powered DNA translocation machine encapsidates the viral genome in the large dsDNA bacteriophages. The essential components include the empty shell, prohead, and the packaging enzyme, terminase. During translocation, terminase is docked on the prohead's portal protein. The translocation ATPase and the concatemer-cutting endonuclease reside in terminase. Remarkably, terminases, portal proteins, and shells of tailed bacteriophages and herpes viruses show conserved features. These DNA viruses may have descended from a common ancestor. Terminase's ATPase consists of a classic nucleotide binding fold, most closely resembling that of monomeric helicases. Intriguing models have been proposed for the mechanism of dsDNA translocation, invoking ATP hydrolysis-driven conformational changes of portal or terminase powering DNA motion. Single-molecule studies show that the packaging motor is fast and powerful. Recent advances permit experiments that can critically test the packaging models. The viral genome translocation mechanism is of general interest, given the parallels between terminases, helicases, and other motor proteins.

Wolbachia are gram-negative bacteria that are widespread in nature, carried by the majority of insect species as well as some mites, crustaceans, and filarial nematodes. Wolbachia can range from parasitic to symbiotic, depending upon the interaction with the host species. The success of Wolbachia is attributed to efficient maternal transmission and manipulations of host reproduction that favor infected females, such as sperm-egg cytoplasmic incompatibility (CI). Much remains unknown about the mechanistic basis for Wolbachia-host interactions. Here we summarize the current understanding of Wolbachia interaction with insect hosts, with a focus on Drosophila. The areas of discussion include Wolbachia transmission in oogenesis, Wolbachia distribution in spermatogenesis, induction and rescue of the CI phenotype, Wolbachia genomics, and Wolbachia-membrane interactions.

For millions of years, retroviral infections have challenged vertebrates, occasionally leading to germline integration and inheritance as ERVs, genetic parasites whose remnants today constitute some 7% to 8% of the human genome. Although they have had significant evolutionary side effects, it is useful to view ERVs as fossil representatives of retroviruses extant at the time of their insertion into the germline and not as direct players in the evolutionary process itself. Expression of particular ERVs is associated with several positive physiological functions as well as certain diseases, although their roles in human disease as etiological agents, possible contributing factors, or disease markers—well demonstrated in animal models—remain to be established. Here we discuss ERV contributions to host genome structure and function, including their ability to mediate recombination, and physiological effects on the host transcriptome resulting from their integration, expression, and other events.

The development of genetic sex determination and cytologically distinct sex chromosomes leads to the potential problem of gene dosage imbalances between autosomes and sex chromosomes and also between males and females. To circumvent these imbalances, mammals have developed an elaborate system of dosage compensation that includes both upregulation and repression of the X chromosome. Recent advances have provided insights into the evolutionary history of how both the imprinted and random forms of X chromosome inactivation have come about. Furthermore, our understanding of the epigenetic switch at the X-inactivation center and the molecular aspects of chromosome-wide silencing has greatly improved recently. Here, we review various facets of the ever-expanding field of mammalian dosage compensation and discuss its evolutionary, developmental, and mechanistic components.