Collateral Damage: Cotton crops that have been bioengineered to express the insecticidal toxin derived from Bacillus thuringiensis (Bt) carry their own insect control, particularly against the cotton bollworm, and are less dependent on externally applied pesticides. Lu et al. (p. 1151 , published online 13 April) now show that reduction in general pesticide use in cotton-growing regions of northern China has shifted the balance of regional pest populations. Bt-expressing cotton now serves as a source of herbivorous insects of the Miridae family, rather than the sink that nonengineered cotton was when less specific pesticides were used. Because these insects will eat a variety of plants, they are emerging as a threat to other crops, including grape, apple, peach, and pear.

Significance: Decades of research have fostered the now-prevalent assumption that noncrop habitat facilitates better pest suppression by providing shelter and food resources to the predators and parasitoids of crop pests. Based on our analysis of the largest pest-control database of its kind, noncrop habitat surrounding farm fields does affect multiple dimensions of pest control, but the actual responses of pests and enemies are highly variable across geographies and cropping systems. Because noncrop habitat often does not enhance biological control, more information about local farming contexts is needed before habitat conservation can be recommended as a viable pest-suppression strategy. Consequently, when pest control does not benefit from noncrop vegetation, farms will need to be carefully comanaged for competing conservation and production objectives.

In tomato (Solanum lycopersicum), as in other plants, the immunity hormone jasmonate (JA) triggers genome-wide transcriptional changes in response to pathogen and insect attack. These changes are largely regulated by the basic helix-loop-helix (bHLH) transcription factor MYC2. The function of MYC2 depends on its physical interaction with the MED25 subunit of the Mediator transcriptional coactivator complex. Although much has been learned about the MYC2-dependent transcriptional activation of JA-responsive genes, relatively less studied is the termination of JA-mediated transcriptional responses and the underlying mechanisms. Here, we report an unexpected function of MYC2 in regulating the termination of JA signaling through activating a small group of JA-inducible bHLH proteins, termed MYC2-TARGETED BHLH1 (MTB1), MTB2, and MTB3. MTB proteins negatively regulate JA-mediated transcriptional responses via their antagonistic effects on the functionality of the MYC2-MED25 transcriptional activation complex. MTB proteins impair the formation of the MYC2-MED25 complex and compete with MYC2 to bind to its target gene promoters. Therefore, MYC2 and MTB proteins form an autoregulatory negative feedback circuit to terminate JA signaling in a highly organized manner. We provide examples demonstrating that gene editing tools such as CRISPR/Cas9 open up new avenues to exploit MTB genes for crop protection.