The nuts and bolts of germ-cell migration

In many species, primordial germ cells (PGCs) migrate from the position where they are specified to the site where the gonad develops, where they differentiate into sperm and egg. Germ cells thus serve as an excellent model for studying cell migration in the context of the live organism. In recent years, a number of cues directing the migration of the cells towards their target were identified and some of the relevant molecules and biochemical pathways were revealed. In this review we present those results, focusing on 'cell mechanics' of the process including cell adhesion, traction generation and cell polarization.     

DNA甲基化的3种可能转录抑制机制

尽管ＤＮＡ甲基化能抑制转录这一观点早已为人所知 ,但其精确的机制还不完全清楚[1] 。到目前为止 ,有 3种可能的机制被用来解释甲基化的转录抑制过程。第一种机制是ＤＮＡ甲基化直接干扰特异转录因子与各自启动子的识别位置结合[2 ] 。几种转录因子 ,如ＡＰ 2、Ｃ Ｍｙｃ/Ｍｙｎ、ＣＡＲＥＢ、Ｅ2Ｆ和ＮＦ κＢ ,能识别含ＣｐＧ残基的序列 ,当ＣｐＧ残基上的Ｃ被甲基化后 ,结合作用即被抑制 (图 1 )。相反 ,其他一些转录因子 (如ＳＰ1和ＣＴＦ)对结合位置上的甲基化不敏感 ,还有许多因子在ＤＮＡ上的结合位点上不含ＣｐＧ二核苷酸 ,ＤＮＡ…     

The nuts and bolts of ring-translocase structure and mechanism

Ring-shaped, oligomeric translocases are multisubunit enzymes that couple the hydrolysis of Nucleoside TriPhosphates (NTPs) to directed movement along extended biopolymer substrates. These motors help unwind nucleic acid duplexes, unfold protein chains, and shepherd nucleic acids between cellular and/or viral compartments. Substrates are translocated through a central pore formed by a circular array of catalytic subunits. Cycles of nucleotide binding, hydrolysis, and product release help reposition translocation loops in the pore to direct movement. How NTP turnover allosterically induces these conformational changes, and the extent of mechanistic divergence between motor families, remain outstanding problems. This review examines the current models for ring-translocase function and highlights the fundamental gaps remaining in our understanding of these molecular machines.     

The nuts and bolts of captive chimpanzee diets and food as enrichment: a survey

Beyond planning for good nutrition, one of the Cornerstones of a successful captive-chimpanzee wellness program is the opportunity for the nonhuman primates to express normal feeding and foraging behaviors. This study presents the results of a survey of 11 institutions—8 zoological and 3 research facilities—given to ascertain how daily diets and feeding enrichments were accomplished. Information represents 806 captive chimpanzees, and entails a composite of captive chimpanzee daily diets, forage and browse materials, periodic treats, medicating and supplemental foods, alternative feeding techniques, and food devices. Results suggest facilities are moving away from timed feeding schedules, which tend to increase prefeeding levels of agonism, to feeding a wide variety of foods throughout the day and using a wide variety of feeding techniques.     

Getting down to malarial nuts and bolts: the interaction between Plasmodium vivax merozoites and their host erythrocytes

Of the four Plasmodium species that routinely cause malaria in humans, Plasmodium falciparum is responsible for the majority of malaria mortality and consequently gets most of the headlines. Outside Africa, however, more malaria cases are caused by its distant cousin Plasmodium vivax, resulting in a daunting morbidity and economic burden for countries across Asia and the Americas. Plasmodium life cycles are complex, but the symptoms and pathology of malaria occur during the blood phase, when merozoites recognize and invade erythrocytes, initiating a developmental programme that culminates in lysis of the erythrocyte and release of multiple daughter merozoites. P. vivax merozoites are dependent on a single host cell receptor for erythrocyte invasion, the Duffy antigen receptor for chemokines, and humans that do not express this receptor on the surface of their erythrocytes are immune to P. vivax infection. This essential receptor-ligand interaction is addressed from both the host and parasite side in two papers in this issue of Molecular Microbiology, with important implications for plans to develop a P. vivax vaccine.