SummaryLateral root development is a post-embryonic organogenesis event that gives rise to most of the underground parts of higher plants. Auxin promotes lateral root formation, but the molecular mechanisms involved are still unknown. We have isolated a novel Arabidopsis mutant, solitary-root (slr), which has reduced sensitivity to auxin. This dominant slr-1 mutant completely lacks lateral roots, and this phenotype cannot be rescued by the application of exogenous auxin. Analysis with cell-cycle and cell-differentiation markers revealed that the slr-1 mutation blocks cell divisions of pericycle cells in lateral root initiation. The slr-1 mutant is also defective in root hair formation and in the gravitropic responses of its roots and hypocotyls. Map-based positional cloning and isolation of an intragenic suppressor mutant revealed that SLR encodes IAA14, a member of the Aux/IAA protein family. Green uorescent protein-tagged mutant IAA14 protein was localized in the nucleus, and the gain-of-function slr-1/iaa14 mutation decreased auxin-inducible BA-GUS gene expression in the root, suggesting that SLR/IAA14 acts as a transcriptional repressor. These observations indicate that SLR/IAA14 is a key regulator in auxin-regulated growth and development, particularly in lateral root formation.

We searched the genomes of eight rice cultivars (Oryza sativa L. ssp. japonica and ssp. indica) and a wild rice accession (Oryza rufipogon Griffith) for nucleotide polymorphisms, and identified 7805 polymorphic loci, including single-nucleotide polymorphisms (SNPs) and insertions/deletions (InDels), in predicted intergenic regions. Polymorphisms are useful as DNA markers for genetic analysis or positional cloning with segregating populations of crosses. Pairwise comparison between cultivars and a neighbor-joining tree calculated from SNPs agreed very well with relationships between rice strains predicted from pedigree data or calculated with other DNA markers such as p-SINE1 and simple sequence repeats (SSRs), suggesting that whole-genome SNP information can be used for analysis of evolutionary relationships. Using multiple SNPs to identify alleles, we drew a map to illustrate the alleles shared among the eight cultivars and the accession. The map revealed that most of the genome is mono- or di-allelic among japonica cultivars, whereas alleles well conserved among modern japonica paddy rice cultivars were often shared with indica cultivars or wild rice, suggesting that the genome structure of modern cultivars is composed of chromosomal segments from various genetic backgrounds. Use of allele-sharing analysis and association analysis were also tested and are discussed.

Mutations in LAMB2 , encoding laminin β 2 , cause Pierson syndrome and occasionally milder nephropathy without extrarenal abnormalities. The most deleterious missense mutations that have been identified affect primarily the N-terminus of laminin β 2 . On the other hand, those associated with isolated nephropathy are distributed across the entire molecule, and variants in the β 2 LEa-LF-LEb domains are exclusively found in cases with isolated nephropathy. Here we report the clinical features of mild isolated nephropathy associated with 3 LAMB2 variants in the LEa-LF-LEb domains (p.R469Q, p.G699R, and p.R1078C) and their biochemical characterization. Although Pierson syndrome missense mutations often inhibit laminin β 2 secretion, the 3 recombinant variants were secreted as efficiently as WT. However, the β 2 variants lost pH dependency for heparin binding, resulting in aberrant binding under physiologic conditions. This suggests that the binding of laminin β 2 to negatively charged molecules is involved in glomerular basement membrane (GBM) permselectivity. Moreover, the excessive binding of the β 2 variants to other laminins appears to lead to their increased deposition in the GBM. Laminin β 2 also serves as a potentially novel cell-adhesive ligand for integrin α 4 β 1 . Our findings define biochemical functions of laminin β 2 variants influencing glomerular filtration that may underlie the pathogenesis of isolated nephropathy caused by LAMB2 abnormalities.