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Jin's two lines of research came together late last year, in work published in the September 4, 2009, issue of Cell. She knew that MAP kinase had to be controlling something else at the synapse, and she and her colleagues found a likely target: it was regulating the speed of messenger RNA (mRNA) decay, which occurs to signal the synapse to reset itself to prepare for the next stimulus. But as far as anyone knew, mRNA was produced in the neuron's main cell body, far from MAP kinase at the synapse.
They predicted that the mRNA existed and was being regulated at the synapse. Long-distance control didn't make sense. Using a second fluorescent marker, they found mRNA molecules were present both in the cell body and at the synapse.
To confirm that mRNA regulation was happening at the synapse, they turned to the femtosecond laser. But when Jin and her colleagues severed an axon in a MAP-kinase-deficient worm, they were startled to see that the neuron couldn't regenerate. The MAP kinase molecule that is so important in creating synapses also appears to play a vital role in rescuing injured neurons.
“The entire MAP kinase pathway is reused in adult neurons,” Jin says. When neurons are injured, it's devastating. “They need to transmit an injury response: regrow your axon, and grow it quickly.” And it happens locally.
Jin is now anxious to manipulate the kinase activity to promote faster injury response, to push the regrowth of injured nerves and guide them to their original target——something essential to restoring function in humans and other species that have much more complex neural systems than worms.
She calls herself impatient, but Jin's persistence and drive are pushing her to solve the ultimate neural puzzle, even if it helps only the worms at first: “I would be totally thrilled if one day, even in C. elegans, an injured axon could completely go back to its normal position.”