Low phosphorus (P) stress limits soybean production. A population of 152 recombinant inbred lines (RILs) derived from a cross between ÔBogaoÕ (P sensitive variety) and ÔNannong 94-156Õ (P tolerant variety) and 248 markers were used to map quantitative trait loci (QTLs) for low-P tolerance. Two pot culture trials were conducted and low-P tolerance evaluated using flower and pod abscission rate under low P and normal P. Conditional QTLs and epistasis for tolerance to low P were also analysed. A conditional QTL (near Satt274) on linkage group D1b+W was identified which conferred low-P tolerance epistatic effects and coincided with previously discovered QTLs. An additive QTL, qFARLPG-07, for flower abscission rate under low P was detected with a LOD score of 7.79 and explained 32.3% of phenotypic variation. It was detected at the same interval of the corresponding QTL for other traits across years. This region coincided with two conditional QTLs (cqFARLPG-07 and cqPARLPG-07), from the P-tolerant parent ÔNannong 94-156Õ related to low-P tolerance. These results will provide a basis for further fine mapping and eventual cloning of the P-efficiency genes in soybean.

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Developmental plasticity is critical for plants to adapt to constantly changing environments. Plant trichomes and root hairs are specialized epidermal cells that paly crucial roles in defense against environmental stressors. Here, we report the isolation of an Arabidopsis mutant, aberrantlybranchedtrichome 6-1 ( abt6-1), with both impaired trichomes and root hairs. Map-based cloning and allelic analyses confirmed that abt6-1 is a new mutant allele of SPIRRIG ( SPI), which encodes a beige and Chediak Higashi (BEACH) domain-containing protein. SPI has been reported to facilitate actin dependent root hair development by temporally and spatially regulating the expression of BRICK1 (BRK1), a subunit of the WAVE/SCAR actin nucleating promoting complex. Based on molecular and biochemical analyses, we found BRK1 is unstable and SPI mediates BRK1 stability. Functional loss of SPI results in the accumulation of steady-state of BRK1. Moreover, we found spi mutant root hairs are hypersensitive to salt stress and their initiation and elongation were entirely inhibited under NaCl treatment. Detailed examination of the actin cytoskeleton revealed that salt stress induces an altered actin organization in root hair and root epidermal cells that resemble those in the spi mutant, implying SPI may respond to salt stress by modulating actin cytoskeleton organization.