蚕豆萎蔫病毒2中国分离物全基因组结构及可能的基因表达方式

报道了蚕豆萎蔫病毒2的B935分离物全基因组序列。RNA1和RNA2分别由5956和3601个核苷酸组成[不包括3‘端未知长度的poly（A）尾巴]。RNA1和RNA2均包含单个阅读框,分别编码分子量为210063（210kD）和119002（119kD）的蛋白质。对外壳蛋白N端氨基酸序列测定表明,外壳蛋白大、小亚基（LCP、SCP）为119kD蛋白质在466／467位的Q／C和868／869位的Q／A位点切割形成的中间和C端蛋白,而端蛋白与豇豆花叶病毒58kD/48kD移动蛋白具有一定的同源性,并且包含一个类似病毒移动蛋白特有的rNTP结合域,推断为移动蛋白。通过与豇豆花叶病毒科病毒RNA1编码的多聚蛋白的同源性比较及功能蛋白保守序列的查找,表明210kd蛋白质可切割形成RdRp、蛋白酶、包含NTP结合域蛋白（NTBM）、蛋白酶辅助因子和Vpg等成熟蛋白,并进一步对其切割位 作了分析,根据LCP和SCP氨基酸序列所作的系统关系树充分证明了蚕豆萎蔫病毒（BBWV）两个血清型,确应命名为两个不同的病毒。     

The evolution of haplodiploidy by male‐killing endosymbionts: importance of population structure and endosymbiont mutualisms

Haplodiploid inheritance systems, characterized by male transmission of only their maternally inherited genomic elements, have evolved more than 20 times within the animal kingdom. A number of theoretical studies have argued that infection with certain male‐killing endosymbionts can potentially lead to the evolution of haplodiploidy. By explicitly investigating the coevolutionary dynamics between host and endosymbiont, we show that the assumptions of current models cannot explain the evolution of haplodiploidy very well, as the endosymbiont will often go extinct in the long term. Here, we provide two additional mechanisms that can explain the stable evolution of haplodiploidy by male‐killing endosymbionts. First of all, a spatially structured population can facilitate the long‐term persistence of haplodiploidy, but this applies only when levels of inbreeding are very high. By contrast, endosymbionts that are mutualistic with their hosts provide a much more general and promising route to the stable evolution of haplodiploidy. This model is the first to provide a formal explanation of the supposed association between the evolution of haplodiploidy and the highly inbred lifestyles of some ancestors, while it also provides a hypothesis for the evolution of haplodiploidy in more outbred ancestors.     

Population biology of a selfish sex ratio distorting element in a booklouse (Psocodea: Liposcelis)

Arthropods harbour a variety of selfish genetic elements that manipulate reproduction to be preferentially transmitted to future generations. A major ongoing question is to understand how these elements persist in nature. In this study, we examine the population dynamics of an unusual selfish sex ratio distorter in a recently discovered species of booklouse, Liposcelis sp. (Psocodea: Liposcelididae) to gain a better understanding of some of the factors that may affect the persistence of this element. Females that carry the selfish genetic element only ever produce daughters, although they are obligately sexual. These females also only transmit the maternal half of their genome. We performed a replicated population cage experiment, varying the initial frequency of females that harbour the selfish element, and following female frequencies for 20 months. The selfish genetic element persisted in all cages, often reaching very high (and thus severely female‐biased) frequencies. Surprisingly, we also found that females that carry the selfish genetic element had much lower fitness than their nondistorter counterparts, with lower lifetime fecundity, slower development and a shorter egg‐laying period. We suggest that differential fitness plays a role in the maintenance of the selfish genetic element in this species. We believe that the genetic system in this species, paternal genome elimination, which allows maternal control of offspring sex ratio, may also be important in the persistence of the selfish genetic element, highlighting the need to consider species with diverse ecologies and genetic systems when investigating the effects of sex ratio manipulators on host populations.     

How to Make a Rodent Giant: Genomic Basis and Tradeoffs of Gigantism in the Capybara,the World’s Largest Rodent

Gigantism results when one lineage within a clade evolves extremely large body size relative to its small-bodied ancestors, a common phenomenon in animals. Theory predicts that the evolution of giants should be constrained by two tradeoffs. First, because body size is negatively correlated with population size, purifying selection is expected to be less efficient in species of large body size, leading to increased mutational load. Second, gigantism is achieved through generating a higher number of cells along with higher rates of cell proliferation, thus increasing the likelihood of cancer. To explore the genetic basis of gigantism in rodents and uncover genomic signatures of gigantism-related tradeoffs, we assembled a draft genome of the capybara (Hydrochoerus hydrochaeris), the world’s largest living rodent. We found that the genome-wide ratio of nonsynonymous to synonymous mutations (ω) is elevated in the capybara relative to other rodents, likely caused by a generation-time effect and consistent with a nearly neutral model of molecular evolution. A genome-wide scan for adaptive protein evolution in the capybara highlighted several genes controlling postnatal bone growth regulation and musculoskeletal development, which are relevant to anatomical and developmental modifications for an increase in overall body size. Capybara-specific gene-family expansions included a putative novel anticancer adaptation that involves T-cell-mediated tumor suppression, offering a potential resolution to the increased cancer risk in this lineage. Our comparative genomic results uncovered the signature of an intragenomic conflict where the evolution of gigantism in the capybara involved selection on genes and pathways that are directly linked to cancer.