Genetic and functional characterization of the rice bacterial blight disease resistance gene xa5.

Xanthomonas oryzae pv. oryzae is the causal agent of rice bacterial blight, a destructive rice disease worldwide. The gene xa5 provides race-specific resistance to X. oryzae pv. oryzae, and encodes the small subunit of transcription factor IIA. How xa5 functions in bacterial blight resistance is not well understood, and its recessive gene action is disputed. Here we show that xa5 is inherited in a completely recessive manner and the susceptible allele Xa5 is fully dominant. In accordance with this, bacterial growth in heterozygous and homozygous susceptible lines is not significantly different. Further, one allele of Xa5 is sufficient to promote disease in previously resistant plants; additional copies are not predictive of increased lesion length. Surprisingly, a resistant nearly isogenic line (NIL) of an indica variety sustains high levels of bacterial populations compared to the susceptible NIL, yet the resistant plants restrict symptom expression. In contrast, in japonica NILs, bacterial population dynamics differ in resistant and susceptible genotypes. However, both resistant indica and japonica plants delay bacterial movement down the leaf. These results support a model in which xa5-mediated recessive resistance is the result of restricted bacterial movement, but not restricted multiplication.

A facelift for the general transcription factor TFIIA.

TFIIA was classified as a general transcription factor when it was first identified. Since then it has been debated to what extent it can actually be regarded as "general". The most notable feature of TFIIA is the proteolytical cleavage of the TFIIAalphabeta into a TFIIAalpha and TFIIAbeta moiety which has long remained a mystery. Recent studies have showed that TFIIA is cleaved by Taspase1 which was initially identified as the protease for the proto-oncogene MLL. Cleavage of TFIIA does not appear to serve as a step required for its activation as the uncleaved TFIIA in the Taspase1 knock-outs adequately support bulk transcription. Instead, cleavage of TFIIA seems to affect its turn-over and may be a part of an intricate degradation mechanism that allows fine-tuning of cellular levels of TFIIA. Cleavage might also be responsible for switching transcription program as the uncleaved and cleaved TFIIA might have distinct promoter specificity during development and differentiation. This review will focus on functional characteristics of TFIIA and discuss novel insights in the role of this elusive transcription factor.

TFIIA plays a role in the response to oxidative stress.

To characterize the role of the general transcription factor TFIIA in the regulation of gene expression by RNA polymerase II, we examined the transcriptional profiles of TFIIA mutants of Saccharomyces cerevisiae using DNA microarrays. Whole-genome expression profiles were determined for three different mutants with mutations in the gene coding for the small subunit of TFIIA, TOA2. Depending on the particular mutant strain, approximately 11 to 27% of the expressed genes exhibit altered message levels. A search for common motifs in the upstream regions of the pool of genes decreased in all three mutants yielded the binding site for Yap1, the transcription factor that regulates the response to oxidative stress. Consistent with a TFIIA-Yap1 connection, the TFIIA mutants are unable to grow under conditions that require the oxidative stress response. Underexpression of Yap1-regulated genes in the TFIIA mutant strains is not the result of decreased expression of Yap1 protein, since immunoblot analysis indicates similar amounts of Yap1 in the wild-type and mutant strains. In addition, intracellular localization studies indicate that both the wild-type and mutant strains localize Yap1 indistinguishably in response to oxidative stress. As such, the decrease in transcription of Yap1-dependent genes in the TFIIA mutant strains appears to reflect a compromised interaction between Yap1 and TFIIA. This hypothesis is supported by the observations that Yap1 and TFIIA interact both in vivo and in vitro. Taken together, these studies demonstrate a dependence of Yap1 on TFIIA function and highlight a new role for TFIIA in the cellular mechanism of defense against reactive oxygen species.