Inheritance of associative memories and acquired cellular changes in C. elegans.

Experiences have been shown to modulate behavior and physiology of future generations in some contexts, but there is limited evidence for inheritance of associative memory in different species. Here, we trained C. elegans nematodes to associate an attractive odorant with stressful starvation conditions and revealed that this associative memory was transmitted to the F1 progeny who showed odor-evoked avoidance behavior.

A negative feedback loop in the GPCR pathway underlies efficient coding of external stimuli.

Efficient navigation based on chemical cues is an essential feature shared by all animals. These cues may be encountered in complex spatiotemporal patterns and with orders of magnitude varying intensities. Nevertheless, sensory neurons accurately extract the relevant information from such perplexing signals.

A Fusion PCR Method for Expressing Genetic Tools in C. elegans.

C. elegans offer a unique opportunity for understanding computation in neural networks. This is largely due to their relatively compact neural network for which a wiring diagram is available.

A Memory Circuit for Coping with Impending Adversity.

Organisms' capacity to anticipate future conditions is key for survival. Associative memories are instrumental for learning from past experiences, yet little is known about the processes that follow memory retrieval and their potential advantage in preparing for impending developments. Here, using C.

A Fusion PCR Method for Expressing Genetic Tools in C. elegans.

C. elegans offer a unique opportunity for understanding computation in neural networks. This is largely due to their relatively compact neural network for which a wiring diagram is available.

Interplay between the DNA damage proteins MDC1 and ATM in the regulation of the spindle assembly checkpoint.

To avoid genomic instability, cells have developed surveillance mechanisms such as the spindle assembly checkpoint (SAC) and the DNA damage response. ATM and MDC1 are central players of the cellular response to DNA double-strand breaks. Here, we identify a new role for these proteins in the regulation of mitotic progression and in SAC activation.

The direct interaction between 53BP1 and MDC1 is required for the recruitment of 53BP1 to sites of damage.

The DNA damage response mediators, 53BP1 and MDC1, play a central role in checkpoint activation and DNA repair. Here we establish that human 53BP1 and MDC1 interact directly through the tandem BRCT domain of MDC1 and residues 1288-1409 of 53BP1. Following induction of DNA double strand breaks the interaction is reduced, probably due to competition between gamma-H2AX and 53BP1 for the binding of the tandem BRCT domain of MDC1.