Yukawa Unification and the Superpartner Mass Scale

Naturalness in supersymmetry (SUSY) is under siege by increasingly stringent LHC constraints, but natural electroweak symmetry breaking still remains the most powerful motivation for superpartner masses within experimental reach. If naturalness is the wrong criterion then what determines the mass scale of the superpartners? We motivate supersymmetry by (1) gauge coupling unification, (2) dark matter, and (3) precision b-tau Yukawa unification. We show that for an LSP that is a bino-Higgsino admixture, these three requirements lead to an upper-bound on the stop and sbottom masses in the several TeV regime because the threshold correction to the bottom mass at the superpartner scale is required to have a particular size. For tan beta about 50, which is needed for t-b-tau unification, the stops must be lighter than 2.8 TeV when A_t has the opposite sign of the gluino mass, as is favored by renormalization group scaling. For lower values of tan beta, the top and bottom squarks must be even lighter. Yukawa unification plus dark matter implies that superpartners are likely in reach of the LHC, after the upgrade to 14 (or 13) TeV, independent of any considerations of naturalness. We present a model-independent, bottom-up analysis of the SUSY parameter space that is simultaneously consistent with Yukawa unification and the hint for m_h = 125 GeV. We study the flavor and dark matter phenomenology that accompanies this Yukawa unification. A large portion of the parameter space predicts that the branching fraction for B_s to mu^+ mu^- will be observed to be significantly lower than the SM value.Comment: 34 pages plus appendices, 20 figure

Pathogenetics of alveolar capillary dysplasia with misalignment of pulmonary veins.

Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a lethal lung developmental disorder caused by heterozygous point mutations or genomic deletion copy-number variants (CNVs) of FOXF1 or its upstream enhancer involving fetal lung-expressed long noncoding RNA genes LINC01081 and LINC01082. Using custom-designed array comparative genomic hybridization, Sanger sequencing, whole exome sequencing (WES), and bioinformatic analyses, we studied 22 new unrelated families (20 postnatal and two prenatal) with clinically diagnosed ACDMPV. We describe novel deletion CNVs at the FOXF1 locus in 13 unrelated ACDMPV patients. Together with the previously reported cases, all 31 genomic deletions in 16q24.1, pathogenic for ACDMPV, for which parental origin was determined, arose de novo with 30 of them occurring on the maternally inherited chromosome 16, strongly implicating genomic imprinting of the FOXF1 locus in human lungs. Surprisingly, we have also identified four ACDMPV families with the pathogenic variants in the FOXF1 locus that arose on paternal chromosome 16. Interestingly, a combination of the severe cardiac defects, including hypoplastic left heart, and single umbilical artery were observed only in children with deletion CNVs involving FOXF1 and its upstream enhancer. Our data demonstrate that genomic imprinting at 16q24.1 plays an important role in variable ACDMPV manifestation likely through long-range regulation of FOXF1 expression, and may be also responsible for key phenotypic features of maternal uniparental disomy 16. Moreover, in one family, WES revealed a de novo missense variant in ESRP1, potentially implicating FGF signaling in the etiology of ACDMPV

Paspalum striate mosaic virus: An Australian mastrevirus from Paspalum dilatatum

Three monocot-infecting mastreviruses from Australia, all found primarily in pasture and naturalised grasses, have been characterised at the molecular level. Here, we present the full genome sequence of a fourth, Paspalum striate mosaic virus (PSMV), isolated from Paspalum dilatatum from south-east Queensland. The genome was 2816 nt long and had an organisation typical of other monocot-infecting mastreviruses. Its nearest relative is Bromus cartharticus striate mosaic virus (BCSMV), with which it shares an overall genome identity of 75%. Phylogenetic analysis of the complete genome and each of the putative viral proteins places PSMV in a group with the other three Australian striate mosaic viruses. PSMV, BCSMV and Digitaria didactyla striate mosaic virus all contain a similar, small recombinant sequence in the small intergenic region