Sterility is common in hybrids between divergent populations, such as the indica and japonica subspecies of Asian cultivated rice (Oryza sativa). Although multiple loci for plant hybrid sterility have been identified, it remains unknown how alleles of the loci interact at the molecular level. Here we show that a locus for indicajaponica hybrid male sterility, Sa, comprises two adjacent genes, SaM and SaF, encoding a small ubiquitin-like modifier E3 ligase-like protein and an F-box protein, respectively. Most indica cultivars contain a haplotype SaM ؉ SaF ؉ , whereas all japonica cultivars have SaM ؊ SaF ؊ that diverged by nucleotide variations in wild rice. Male semi-sterility in this heterozygous complex locus is caused by abortion of pollen carrying SaM ؊ . This allele-specific gamete elimination results from a selective interaction of SaF ؉ with SaM ؊ , a truncated protein, but not with SaM ؉ because of the presence of an inhibitory domain, although SaM ؉ is required for this male sterility. Lack of any one of the three alleles in recombinant plants does not produce male sterility. We propose a two-gene/threecomponent interaction model for this hybrid male sterility system. The findings have implications for overcoming male sterility in inter-subspecific hybrid rice breeding.allelic interaction ͉ gamete selection ͉ hybrid sterility ͉ reproductive barrier ͉ two-gene/three-component model

Most root traits in soybean were conditioned by more than two minor QTLs. The region closer to Satt519 on the B1 linkage group might have great potential for future genetic improvement for soybean P efficiency through root selection.

Although quantitative trait loci (QTL) underpin many desirable agronomic traits, their incorporation into crop plants through marker-assisted selection is limited by the low predictive value of markers on phenotypic performance. Here we used candidate defense response (DR) genes to dissect quantitative resistance in rice using recombinant inbred (RI) and advanced backcross (BC) populations derived from a blast-resistant cultivar, Sanhuangzhan 2 (SHZ-2). Based on DNA profiles of DR genes, RI lines were clustered into two groups corresponding to level of resistance. Five DR genes, encoding putative oxalate oxidase, dehydrin, PR-1, chitinase, and 14-3-3 protein, accounted for 30.0, 23.0, 15.8, 6.7, and 5.5% of diseased leaf area (DLA) variation, respectively. Together, they accounted for 60.3% of the DLA variation and co-localized with resistance QTL identified by interval mapping. Average phenotypic contributions of oxalate oxidase, dehydrin, PR-1, chitinase, and 14-3-3 protein in BC lines were 26.1, 19.0, 18.0, 11.5, and 10.6%, respectively, across environments. Advanced BC lines with four to five effective DR genes showed enhanced resistance under high disease pressure in field tests. Our results demonstrate that the use of natural variation in a few candidate genes can solve a long-standing problem in rice production and has the potential to address other problems involving complex traits.

Different rabies virus (RABV) strains have their own biological characteristics, but little is known about their respective impact on autophagy. Therefore, we evaluated whether attenuated RABV HEP-Flury and wildtype RABV GD-SH-01 strains triggered autophagy. We found that GD-SH-01 infection significantly increased the number of autophagy-like vesicles, the accumulation of enhanced green fluorescent protein (EGFP)-LC3 fluorescence puncta and the conversion of LC3-I to LC3-II, while HEP-Flury was not able to induce this phenomenon. When evaluating autophagic flux, we found that GD-SH-01 infection triggers a complete autophagic response in the human neuroblastoma cell line (SK), while autophagosome fusion with lysosomes was inhibited in a mouse neuroblastoma cell line (NA). In these cells, GD-SH-01 led to apoptosis and mitochondrial dysfunction while triggering autophagy, and apoptosis could be decreased by enhancing autophagy. To further identify the virus constituent causing autophagy, 5 chimeric recombinant viruses carrying single genes of HEP-Flury instead of those of GD-SH-01 were rescued. While the HEP-Flury virus carrying the wild-type matrix protein (M) gene of RABV triggered LC3-I to LC3-II conversion in SK and NA cells, replacement of genes of nucleoprotein (N), phosphoprotein (P) and glycoprotein (G) produced only minor autophagy. But no one single structural protein of GD-SH-01 induced autophagy. Moreover, the AMPK signaling pathway was activated by GD-SH-01 in SK. Therefore, our data provide strong evidence that autophagy is induced by GD-SH-01 and can decrease apoptosis in vitro. Furthermore, the M gene of GD-SH-01 may cooperatively induce autophagy.