A mechanistic framework for auxin dependent Arabidopsis root hair elongation to low external phosphate

Phosphate (P) is an essential macronutrient for plant growth. Roots employ adaptive mechanisms to forage for P in soil. Root hair elongation is particularly important since P is immobile. Here we report that auxin plays a critical role promoting root hair growth in Arabidopsis in response to low external P. Mutants disrupting auxin synthesis (taa1) and transport (aux1) attenuate the low P root hair response. Conversely, targeting AUX1 expression in lateral root cap and epidermal cells rescues this low P response in aux1. Hence auxin transport from the root apex to differentiation zone promotes auxin-dependent hair response to low P. Low external P results in induction of root hair expressed auxin-inducible transcription factors ARF19, RSL2, and RSL4. Mutants lacking these genes disrupt the low P root hair response. We conclude auxin synthesis, transport and response pathway components play critical roles regulating this low P root adaptive response

Systematic screening for skin, hair, and nail abnormalities in a large-scale knockout mouse program

The International Knockout Mouse Consortium was formed in 2007 to inactivate (“knockout”) all protein-coding genes in the mouse genome in embryonic stem cells. Production and characterization of these mice, now underway, has generated and phenotyped 3,100 strains with knockout alleles. Skin and adnexa diseases are best defined at the gross clinical level and by histopathology. Representative retired breeders had skin collected from the back, abdomen, eyelids, muzzle, ears, tail, and lower limbs including the nails. To date, 169 novel mutant lines were reviewed and of these, only one was found to have a relatively minor sebaceous gland abnormality associated with follicular dystrophy. The B6N(Cg)-Far2tm2b(KOMP)Wtsi/2J strain, had lesions affecting sebaceous glands with what appeared to be a secondary follicular dystrophy. A second line, B6N(Cg)-Ppp1r9btm1.1(KOMP)Vlcg/J, had follicular dystrophy limited to many but not all mystacial vibrissae in heterozygous but not homozygous mutant mice, suggesting that this was a nonspecific background lesion. We discuss potential reasons for the low frequency of skin and adnexal phenotypes in mice from this project in comparison to those seen in human Mendelian diseases, and suggest alternative approaches to identification of human disease-relevant models.This work was supported by grants from the National Institutes of Health (R21-AR063781 and U42-OD011185). Shared services at The Jackson Laboratory are subsidized by a National Cancer Institute Core Grant (P30-CA034196). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

Measurement of W-pair production in e+e−e^+ e^- collisions at 189 GeV

The production of W-pairs is analysed in a data samplecollected by ALEPH at a mean centre-of-mass energy of 188.6 GeV,corresponding to an integrated luminosity of 174.2 pb^-1. Crosssections are given for different topologies of W decays intoleptons or hadrons. Combining all final states and assumingStandard Model branching fractions, the total W-pair cross sectionis measured to be 15.71 +- 0.34 (stat) +- 0.18 (syst) pb.Using also the W-pair data samples collected by ALEPH at lowercentre-of-mass energies, the decay branching fraction of the W bosoninto hadrons is measured to be BR (W hadrons) = 66.97+- 0.65 (stat) +- 0.32 (syst) %, allowing a determination of theCKM matrix element |V(cs)|= 0.951 +- 0.030 (stat) +- 0.015 (syst)

Searches for neutral Higgs bosons in e+e−e^{+}e^{-} collisions at centre-of-mass energies from 192 to 202 GeV

Searches for neutral Higgs bosons are performed with the 237 pb^-1 of data collected in 1999 by the ALEPH detector at LEP, for centre-of-mass energies between 191.6 and 201.6 GeV. These searches apply to Higgs bosons within the context of the Standard Model and its minimal supersymmetric extension (MSSM) as well as to invisibly decaying Higgs bosons. No evidence of a signal is seen. A lower limit on the mass of the Standard Model Higgs boson of 107.7 GeV/c^2 at 95% confidence level is set. In the MSSM, lower limits of 91.2 and 91.6 GeV/c^2 are derived for the masses of the neutral Higgs bosons h and A, respectively. For a Higgs boson decaying invisibly and produced with the Standard Model cross section, masses below 106.4 GeV/c^2 are excluded

Measurement of the W mass by direct reconstruction in e+e−e^+ e^- collisions at 172 GeV

The mass of the W boson is obtained from reconstructed invariant mass distributions in W-pair events. The sample of W pairs is selected from 10.65~pb$^{-1}$ collected with the ALEPH detector at a mean centre-of-mass energy of 172.09 \GEV. The invariant mass distribution of simulated events are fitted to the experimental distributions and the following W masses are obtained: $WW \to q\overline{q}q\overline{q } m_W = 81.30 +- 0.47(stat.) +- 0.11(syst.) GeV/c^2$, $WW \to l\nu q\overline{q}(l=e,\mu) m_W = 80.54 +- 0.47(stat.) +- 0.11(syst.) GeV/c^2$, $WW \to \tau\nu q\overline{q} m_W = 79.56 +- 1.08(stat.) +- 0.23(syst.) GeV/C62$. The statistical errors are the expected errors for Monte Carlo samples of the same integrated luminosity as the data. The combination of these measurements gives: $m_W = 80.80 +- 0.11(syst.) +- 0.03(LEP energy) GeV/^2$