NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants.

Salicylic acid (SA) is a plant immune signal produced after pathogen challenge to induce systemic acquired resistance. It is the only major plant hormone for which the receptor has not been firmly identified. Systemic acquired resistance in Arabidopsis requires the transcription cofactor nonexpresser of PR genes 1 (NPR1), the degradation of which acts as a molecular switch. Here we show that the NPR1 paralogues NPR3 and NPR4 are SA receptors that bind SA with different affinities. NPR3 and NPR4 function as adaptors of the Cullin 3 ubiquitin E3 ligase to mediate NPR1 degradation in an SA-regulated manner. Accordingly, the Arabidopsis npr3 npr4 double mutant accumulates higher levels of NPR1, and is insensitive to induction of systemic acquired resistance. Moreover, this mutant is defective in pathogen effector-triggered programmed cell death and immunity. Our study reveals the mechanism of SA perception in determining cell death and survival in response to pathogen challenge.

The neural substrates responsible for food odor processing: an activation likelihood estimation meta-analysis.

In many species including humans, food odors appear to play a distinct role when compared with other odors. Despite their functional distinction, the neural substrates responsible for food odor processing remain unclear in humans. This study aimed to identify brain regions involved in food odor processing using activation likelihood estimation (ALE) meta-analysis. We selected olfactory neuroimaging studies conducted with sufficient methodological validity using pleasant odors. We then divided the studies into food and non-food odor conditions. Finally, we performed an ALE meta-analysis for each category and compared the ALE maps of the two categories to identify the neural substrates responsible for food odor processing after minimizing the confounding factor of odor pleasantness. The resultant ALE maps revealed that early olfactory areas are more extensively activated by food than non-food odors. Subsequent contrast analysis identified a cluster in the left putamen as the most likely neural substrate underlying food odor processing. In conclusion, food odor processing is characterized by the functional network involved in olfactory sensorimotor transformation for approaching behaviors to edible odors, such as active sniffing.

MYC-type transcription factors, MYC67 and MYC70, interact with ICE1 and negatively regulate cold tolerance in Arabidopsis.

The expression of hundreds of genes is induced by low temperatures via a cold signaling pathway. ICE1, a MYC-type transcription factor, plays an important role in the induction of CBF3/DREB1A to control cold-responsive genes and cold tolerance. To elucidate other molecular factors, a yeast 2-hybrid screening was performed. Two MYC-type transcription factors, MYC67 and MYC70, were identified as ICE1-interacting proteins. The myc mutants were more tolerant to freezing temperatures than wild type. CBF3/DREB1A and other cold-responsive genes were up-regulated in the myc mutants. Overexpression of the MYC genes increased the cold sensitivity and down-regulated the expression of cold-responsive genes. The MYC proteins interacted with the cis-elements in the CBF3/DREB1A promoter, probably to interfere interaction between ICE1 and the cis-elements. Taken together, these results demonstrate that MYC67 and MYC70, ICE1 interactors, negatively regulate cold-responsive genes and cold tolerance.

The HSF-like transcription factor TBF1 is a major molecular switch for plant growth-to-defense transition.

BACKGROUND: Induction of plant immune responses involves significant transcription reprogramming that prioritizes defense over growth-related cellular functions. Despite intensive forward genetic screens and genome-wide expression-profiling studies, a limited number of transcription factors have been found that regulate this transition. RESULTS: Using the endoplasmic-reticulum-resident genes required for antimicrobial protein secretion as markers, we identified a heat-shock factor-like transcription factor that specifically binds to the TL1 (GAAGAAGAA) cis element required for the induction of these genes. Surprisingly, plants lacking this TL1-binding factor, TBF1, respond normally to heat stress but are compromised in immune responses induced by salicylic acid and by microbe-associated molecular pattern, elf18. Genome-wide expression profiling indicates that TBF1 plays a key role in the growth-to-defense transition. Moreover, the expression of TBF1 itself is tightly regulated at both the transcriptional and translational levels. Two upstream open reading frames encoding multiple aromatic amino acids were found 5' of the translation initiation codon of TBF1 and shown to affect its translation. CONCLUSIONS: Through this unique regulatory mechanism, TBF1 can sense the metabolic changes upon pathogen invasion and trigger the specific transcriptional reprogramming through its target genes expression.