These findings raise many fascinating questions. How are all these different stimulus features encoded at the level of gene expression in this one neuron pair?

Many of these genes are AFD-specific but controlled by broadly expressed #activity-dependent programs. How do the activity-regulated and cell identity programs interact to drive these gene batteries? What do all these genes DO? And more. 8/n

Also cool - a pyt-1 allele with just one upstream CREB site mutated has same plasticity defects as pyt-1 null.

This means that the large magnitude temperature upshift works via CREB to directly upregulate pyt-1 so that AFD is able to change its response properties and drive behavioral plasticity specifically under these conditions. (See 3rd post in 🧵 ). 7/n

The gene #regulatory program is complex as expected, and is in part mediated by the usual suspects – calcium channels, CaMK and direct and indirect regulation by the #CREB transcription factor.

But does this differential regulation mean anything for AFD functions in response to specific temperature experiences? Yes!

Levels of the DAC-1 TF read out absolute warm growth temperature & this TF regulates the warm temperature-driven decision to enter the dauer stage. 5/n