Cellular and genetic responses to mesoderm induction in Xenopus

Mesodermal cell differentiation begins in response to an inductive interaction early in frog development. In parallel with the recent finding that certain peptide growth factors can induce mesoderm, early cellular and genetic responses to the induction have been discovered. I review here recent work on these responses, work that aims to understand how cells respond to inducers to form the complex pattern of the vertebrate mesoderm.     

New gene assignments using a complete, characterized sheep-hamster somatic cell hybrid panel

The generation and characterization of new sheep-hamster cell hybrids is reported from the fusion of sheep white blood cells with six different hamster auxotrophs. Selection from these and previously generated cell hybrids has led to the production of a panel of 30 hybrids covering the complete sheep genome of 28 chromosomes. Over half of the cell hybrids in this panel contain single sheep chromosomes. By complementation, the following new assignments have been made using the panel: phosphoribosyl N-formylglycinamide amidotransferase (PRFGA) to sheep chromosome (chr) 11; adenylosuccinate synthetase (ADSS) to sheep chr 12; adenylosuccinate lyase (ADSL) to sheep chr 3q; 3-hydroxy-3-methylglutaryl-coenzyme A synthase (HMGCS) to sheep chr 16; dihydrofolate reductase (DHFR) to sheep chr 5; and adenine phosphoribosyltransferase (APRT) to sheep chr 14. The gene phosphoribosylaminoinidazole-carboxamide formyltransferase/Inosinicase (PRACFT) has now been regionally assigned to chr 2q. By isozyme analysis, phosphogluconate dehydrogenase (PGD) was assigned to sheep chr 12, anchoring the sheep syntenic group U1 to this chromosome, and mannose phosphate isomerase (MPI) was assigned to sheep chr 18. Furthermore, the chromosomal assignment of 110 microsatellites was confirmed using this cell panel.     

Host-Parasite Interactions and Purifying Selection in a Microsporidian Parasite of Honey Bees

To clarify the mechanisms of Nosema ceranae parasitism, we deep-sequenced both honey bee host and parasite mRNAs throughout a complete 6-day infection cycle. By time-series analysis, 1122 parasite genes were significantly differently expressed during the reproduction cycle, clustering into 4 expression patterns. We found reactive mitochondrial oxygen species modulator 1 of the host to be significantly down regulated during the entire infection period. Our data support the hypothesis that apoptosis of honey bee cells was suppressed during infection. We further analyzed genome-wide genetic diversity of this parasite by comparing samples collected from the same site in 2007 and 2013. The number of SNP positions per gene and the proportion of non-synonymous substitutions per gene were significantly reduced over this time period, suggesting purifying selection on the parasite genome and supporting the hypothesis that a subset of N. ceranae strains might be dominating infection.     

Does maternal condition or predation risk influence small mammal population dynamics?

There is strong debate over whether the intrinsic traits of individuals or the extrinsic environment exert the greater influence on small mammal population dynamics. We test the roles of maternal effects (an intrinsic factor) and predation risk (an extrinsic factor) in the population dynamics of wild strain house mice using a 2-factor enclosure experiment. Pre-release supplemental feeding with a high-fat diet created female treatment founders that were 6–10% heavier than controls, a condition that we predicted would be passed on as a maternal effect. Predation risk was enhanced using regular application of predator (red fox Vulpes vulpes ) scats. Founder populations of six females and six males released into eight, 15×15 m enclosures showed near exponential population growth over 17 weeks (maximum 3 generations). But there were no responses to either treatment in terms of survival, inherited body weights, fecundity or population size. We suggest that elevated maternal condition may have only minor and transient intergenerational effects with little long-term consequence. We also suggest that the general significance of predator scats as a cue to predation risk to alter prey behaviour may have been overestimated. Hence our results question the role of either factor in causing long-term responses that influence condition to affect population processes.