Identification of a Novel QTL for Chlorate Resistance in Rice (Oryza sativa L.)

Chlorate resistance analysis is an effective approach commonly used to distinguish the genetic variation between Oryza sativa L. ssp. indica and japonica, and predict the nitrogen use efficiency (NUE). This study aimed at investigating the response of a doubled haploid (DH) population derived from anther culture of 93-11 × Milyang352 exposed to 0.1% potassium chlorate (KClO3) at the seedling stage. The results revealed that the parental rice lines 93-11 (indica) and Milyang352 (japonica) showed distinctive phenotypic responses. The parental line 93-11 scored highly sensitive (0% survival) and Milyang352 scored resistant (66.7% survival) 7 days after treatment. The DH lines reflected the differential phenotypic response observed in parental lines. Interestingly, we identified a novel quantitative trait locus (QTL) for chlorate resistance on chromosome 3 (qCHR-3, 136 cM, logarithm of the odds—LOD: 4.1) using Kompetitive Allele-Specific PCR (KASP) markers. The additive effect (−11.97) and phenotypic variation explained (PVE; 14.9%) indicated that the allele from Milyang352 explained the observed phenotypic variation. In addition, shoot growth showed a significant difference between parental lines, but not root growth. Moreover, in silico analysis identified candidate genes with diverse and interesting molecular and physiological functions. Therefore, this study suggested that the QTL qCHR-3 harbors promising candidate genes that could play a role in the regulation of nitrogen metabolism in rice.

The effects of chlorate- and streptomycin-resistance mutations on nitrofurantoin resistance in Escherichia coli K-12

Chlorate-resistant mutants with none of the usual pleiotropic effects such as defective nitrate reductase activity were isolated from Escherichia coli K-12. These chlorate-resistant mutants (designated chlHW) did not yield strains with a high level of nitrofurantoin resistance following selection with nitrofurantoin. The chlorate-resistance mutation reduced the nitrofurantoin resistance of high-level mutants to an intermediate level. Further mutation to resistance to streptomycin and other aminoglycoside antibiotics suppressed the effect of chlHW on the level of nitrofurantoin resistance. Other chlorate-resistance genes examined did not have the same effect on nitrofurantoin resistance as chlHW. The gene was cotransducible (P1) with intermediate-level nitrofurantoin resistance and proC. It is suggested that the chlHW mutation may enhance the accumulation of nitrofurantoin inside the cell since it is known that a multiple aminoglycoside-resistance mutation with pleiotropic effects on the cell membrane can also confer high-level resistance to nitrofurantoin.