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297 Rapid and economic mapping of regulatory loci in complex traits using gene expression<br />

profiling<br />

Remco Van Poecke, Masanao Sato, Lisa Lenarz-Wyatt, Fumiaki Katagiri<br />

University of Minnesota<br />

Genetic variation is a useful tool to dissect complex traits, such as inducible defense against pathogens in plants.<br />

An excellent source of genetic variation can be found in naturally occurring populations. However, use of such natural<br />

variation is hampered by the quantitative nature of complex traits. Thus, dissection of complex traits using natural<br />

variation commonly involved tedious genetic crossing schemes and genotypic analyses, such as creation, phenotyping,<br />

and genotyping of recombinant inbred lines. We are currently developing a rapid and economical method to detect and<br />

map regulatory loci involved in complex traits. The concept of this method is to finely dissect the phenotype for a complex<br />

trait using expression profiles and to identify parts of phenotype (i.e., expression of some genes) that segregate in a<br />

Mendelian manner and that are controlled in trans. We initiated characterization of Arabidopsis accessions in response<br />

to infection of an avirulent bacterial strain by conventional phenotyping and expression profiling. To reduce the cost of<br />

expression profiling, we are using a dedicated small-scale DNA microarray. We will report that the dedicated microarray<br />

is an excellent tool to study natural variation in Arabidopsis and that results of the phenotypic and expression profile<br />

characterization of the parental accessions are well correlated.<br />

This project was supported by the National Research Initiative of the USDA Cooperative State Research, Education<br />

and Extension Service, grant number 2004-35301-14525.<br />

298 Arabidopsis Bax-Inhibitor 1 Functions As An Attenuator Of Biotic And Abiotic Types of Cell<br />

Death<br />

Naohide Watanabe, Eric Lam<br />

Biotech Center, Rutgers The State University of New Jersey<br />

Programmed cell death (PCD) is a common process in eukaryotes during development and in response to pathogens<br />

and stress signals. Bax inihibitor-1 (BI-1) is a small protein of 25-27 kDa <strong>with</strong> 6 or 7 predicted transmembrane domains<br />

and is mainly localized in the membrane of the endoplasmic reticulum (ER). BI-1 is proposed to be a cell death suppressor<br />

that is conserved in both animals and plants, but the physiological importance of BI-1 and the impact of its loss of function<br />

in plants are still unclear. In this study, we identified and characterized two independent Arabidopsis mutants <strong>with</strong> a<br />

T-DNA insertion in the AtBI1 gene. The phenotype of atbi1-1 and atbi1-2, <strong>with</strong> a C-terminal missense mutation and a<br />

gene knockout, respectively, was indistinguishable from wild-type plants under normal growth conditions. However,<br />

these two mutants exhibit accelerated progression of cell death upon infiltration of leaf tissues <strong>with</strong> a PCD-inducing<br />

fungal toxin fumonisin B1 (FB1) and increased sensitivity to heat shock-induced cell death. Under these conditions,<br />

expression of AtBI1 mRNA was up-regulated in wild-type leaves prior to the activation of cell death, suggesting that<br />

increase of AtBI1 expression is important for basal suppression of cell death progression. Overexpression of AtBI1 in the<br />

two homozygous mutant backgrounds rescued the accelerated cell death phenotypes. In addition, we found that AtBI1<br />

expression is enhanced under the ER stress conditions, suggesting that AtBI1 could modulate ER stress-induced cell<br />

death. Together, our results provide direct genetic evidence for a role of BI-1 as an attenuator for cell death progression<br />

triggered by both biotic and abiotic types of cell death signals in Arabidopsis.<br />

N. Watanabe & E. Lam (2006) Arabidopsis Bax Inhibitor-1 functions as an attenuator of biotic and abiotic types of cell death. Plant Journal<br />

45(6):884-894.

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