Non-PORC behaviour of a class of descendant pp-groups

We prove that the number of immediate descendants of order $p^10$ of $G_p$ is not PORC (Polynomial On Residue Classes) where $G_p$ is the $p$-group of order $p^9$ defined by du Sautoy's nilpotent group encoding the elliptic curve $y^2=x^3-x$. This has important implications for Higman's PORC conjecture

Auxin and tryptophan homeostasis are facilitated by the ISS1/VAS1 aromatic aminotransferase in arabidopsis

Indole-3-acetic acid (IAA) plays a critical role in regulating numerous aspects of plant growth and development. While there is much genetic support for tryptophan-dependent (Trp-D) IAA synthesis pathways, there is little genetic evidence for tryptophan-independent (Trp-I) IAA synthesis pathways. Using Arabidopsis, we identified two mutant alleles of ISS1 ( I: ndole S: evere S: ensitive) that display indole-dependent IAA overproduction phenotypes including leaf epinasty and adventitious rooting. Stable isotope labeling showed that iss1, but not WT, uses primarily Trp-I IAA synthesis when grown on indole-supplemented medium. In contrast, both iss1 and WT use primarily Trp-D IAA synthesis when grown on unsupplemented medium. iss1 seedlings produce 8-fold higher levels of IAA when grown on indole and surprisingly have a 174-fold increase in Trp. These findings indicate that the iss1 mutant's increase in Trp-I IAA synthesis is due to a loss of Trp catabolism. ISS1 was identified as At1g80360, a predicted aromatic aminotransferase, and in vitro and in vivo analysis confirmed this activity. At1g80360 was previously shown to primarily carry out the conversion of indole-3-pyruvic acid to Trp as an IAA homeostatic mechanism in young seedlings. Our results suggest that in addition to this activity, in more mature plants ISS1 has a role in Trp catabolism and possibly in the metabolism of other aromatic amino acids. We postulate that this loss of Trp catabolism impacts the use of Trp-D and/or Trp-I IAA synthesis pathways.T32 AR059033 - NIAMS NIH HH

Local lung hypoxia determines epithelial fate decisions during alveolar regeneration.

After influenza infection, lineage-negative epithelial progenitors (LNEPs) exhibit a binary response to reconstitute epithelial barriers: activating a Notch-dependent ΔNp63/cytokeratin 5 (Krt5) remodelling program or differentiating into alveolar type II cells (AEC2s). Here we show that local lung hypoxia, through hypoxia-inducible factor (HIF1α), drives Notch signalling and Krt5pos basal-like cell expansion. Single-cell transcriptional profiling of human AEC2s from fibrotic lungs revealed a hypoxic subpopulation with activated Notch, suppressed surfactant protein C (SPC), and transdifferentiation toward a Krt5pos basal-like state. Activated murine Krt5pos LNEPs and diseased human AEC2s upregulate strikingly similar core pathways underlying migration and squamous metaplasia. While robust, HIF1α-driven metaplasia is ultimately inferior to AEC2 reconstitution in restoring normal lung function. HIF1α deletion or enhanced Wnt/β-catenin activity in Sox2pos LNEPs blocks Notch and Krt5 activation, instead promoting rapid AEC2 differentiation and migration and improving the quality of alveolar repair

The seasonal cycle of ocean-atmosphere CO2 Flux in Ryder Bay, West Antarctic Peninsula

Approximately 15 million km2 of the Southern Ocean is seasonally ice covered, yet the processes affecting carbon cycling and gas exchange in this climatically important region remain inadequately understood. Here, 3 years of dissolved inorganic carbon (DIC) measurements and carbon dioxide (CO2) fluxes from Ryder Bay on the west Antarctic Peninsula (WAP) are presented. During spring and summer, primary production in the surface ocean promotes atmospheric CO2 uptake. In winter, higher DIC, caused by net heterotrophy and vertical mixing with Circumpolar Deep Water, results in outgassing of CO2 from the ocean. Ryder Bay is found to be a net sink of atmospheric CO2 of 0.59–0.94 mol C m−2 yr−1 (average of 3 years). Seasonal sea ice cover increases the net annual CO2 uptake, but its effect on gas exchange remains poorly constrained. A reduction in sea ice on the WAP shelf may reduce the strength of the oceanic CO2 sink in this region