Mutational analysis of the Arabidopsis RPS2 disease resistance gene and the corresponding pseudomonas syringae avrRpt2 avirulence gene.

Plants have evolved a large number of disease resistance genes that encode proteins containing conserved structural motifs that function to recognize pathogen signals and to initiate defense responses. The Arabidopsis RPS2 gene encodes a protein representative of the nucleotide-binding site-leucine-rich repeat (NBS-LRR) class of plant resistance proteins. RPS2 specifically recognizes Pseudomonas syringae pv. tomato strains expressing the avrRpt2 gene and initiates defense responses to bacteria carrying avrRpt2, including a hypersensitive cell death response (HR). We present an in planta mutagenesis experiment that resulted in the isolation of a series of rps2 and avrRpt2 alleles that disrupt the RPS2-avrRpt2 gene-for-gene interaction. Seven novel avrRpt2 alleles incapable of eliciting an RPS2-dependent HR all encode proteins with lesions in the C-terminal portion of AvrRpt2 previously shown to be sufficient for RPS2 recognition. Ten novel rps2 alleles were characterized with mutations in the NBS and the LRR. Several of these alleles code for point mutations in motifs that are conserved among NBS-LRR resistance genes, including the third LRR, which suggests the importance of these motifs for resistance gene function.

The helicase domain of the TMV replicase proteins induces the N-mediated defence response in tobacco.

Tobacco mosaic virus (TMV) induces the hypersensitive response (HR) in tobacco plants containing the N gene. This defence response is characterized by cell death at the site of virus infection and inhibition of viral replication and movement. A previous study indicated that a portion of the TMV replicase containing a putative helicase domain is involved in HR induction. Here, this observation is confirmed and extended by showing that non-viral expression of a 50 kDa TMV helicase fragment (p50) is sufficient to induce the N-mediated HR in tobacco. Like the HR elicited by TMV infection, transgenic expression of p50 induces a temperature-sensitive defence response. We demonstrate that recombinant p50 protein has ATPase activity, as suggested by the presence of conserved sequence motifs found in ATPase/helicase enzymes. A point mutation that alters one of these motifs abolishes ATPase activity in vitro but does not affect HR induction. These results suggest that features of the TMV helicase domain, independent of its enzymatic activity, are recognized by N-containing tobacco to induce TMV resistance.

Plasma leptin decreases during lactation in insectivorous bats.

We previously demonstrated high leptin levels during late pregnancy in little brown bats (Myotis lucifugus). We now extend these observations to a second species, the big brown bat (Eptesicus fuscus), and also report that leptin increases after the first trimester of pregnancy. Leptin decreased to baseline 1 week following parturition, with a half-time decay of 2 days. During lactation, leptin was significantly correlated with body mass in E. fuscus, but not in M. lucifugus. No circadian pattern of leptin was observed in M. lucifugus. The decrease in post-partum leptin in bats may be partly explained by loss of putative placental leptin. The continued decrease may reflect depletion of body fat during this energy demanding period, at least in Eptesicus. Changes in leptin during lactation appeared to be independent of circadian effects and time of sampling. Our study provides additional evidence that leptin increases during pregnancy and declines during lactation in a free-ranging mammal, supporting the hypothesis that leptin plays important but yet undetermined roles in reproduction.