Intracellular amastigotes of the Chagas disease agent Trypanosoma cruzi can spontaneously enter an extended state of replicative dormancy, during which time they are resistant to drug treatment both in vitro and in vivo.
Analyses of cell type-specific data show that the maternal alleles of genes related to establishing and breaking seed dormancy are suppressed by different combinations of epigenetic marks in the endosperm of Arabidopsis.
Inhibition enhances the spatial specificity of high calcium influx for cooperatively stimulated synapses, suggesting that inhibitory inputs may regulate both synapse-specific and heterosynaptic plasticity to support learning and memory.
Natural variation for an adaptively important life history trait is largely due to variation at a single, major-effect locus with multiple alleles, demonstrating that not all complex traits are massively polygenic.
This comprehensive transcriptomic resource of dormant and replicating malaria liver parasites highlights the dearth of pathways that operate in the hypnozoites and the need to investigate druggability (i.e. selectivity and safety) of core pathways in malaria parasites.
Transcriptome profiling of malaria liver-stage parasites provides unprecedented knowledge on genes and pathways expressed in truly dormant hypnozoites and indicates that dormancy is associated with a switch in energy metabolism.