On the topology of the permutation pattern poset

The set of all permutations, ordered by pattern containment, forms a poset. This paper presents the first explicit major results on the topology of intervals in this poset. We show that almost all (open) intervals in this poset have a disconnected subinterval and are thus not shellable. Nevertheless, there seem to be large classes of intervals that are shellable and thus have the homotopy type of a wedge of spheres. We prove this to be the case for all intervals of layered permutations that have no disconnected subintervals of rank 3 or more. We also characterize in a simple way those intervals of layered permutations that are disconnected. These results carry over to the poset of generalized subword order when the ordering on the underlying alphabet is a rooted forest. We conjecture that the same applies to intervals of separable permutations, that is, that such an interval is shellable if and only if it has no disconnected subinterval of rank 3 or more. We also present a simplified version of the recursive formula for the M\"obius function of decomposable permutations given by Burstein et al.Comment: 33 pages, 4 figures. Incorporates changes suggested by the referees; new open problems in Subsection 9.4. To appear in JCT(A

Evaluating a model of global psychophysical judgments for brightness: II. Behavioral properties linking summations and productions

Steingrimsson (Attention, Perception, & Psychophysics, 71, 1916–1930, 2009) outlined Luce’s (Psychological Review, 109, 520–532 2002, 111, 446–454 2004) proposed psychophysical theory and tested, for brightness, behavioral properties that, separately, gave rise to two psychophysical functions, Ψ⊕ and \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\Psi_{{ \circ_p}}}$$\end{document}. The function Ψ⊕ maps pairs of physical intensities onto positive real numbers and represents subjective summation, and the function \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\Psi_{{ \circ_p}}}$$\end{document} represents a form of ratio production. This article, the second in a series expected to consist of three articles, tests the properties linking summation and production such that it forces \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${\Psi_{{ \circ_p}}} = {\Psi_\oplus } = \Psi$$\end{document}. The properties tested are a form of distributivity and, in three experiments, were subjected to an empirical evaluation. Considerable support is provided for the existence of a single function Ψ for both summation and ratio production. The scope of this series of articles is to establish the theory as a descriptive model of binocular brightness perception

Changes in the Expression of Myosins During Postnatal Development of Masseter Muscle in the Microphthalmic Mouse

In the present study, to elucidate the influences of the deficiency of teeth on the masseter muscle, we analyzed changes in the expression of MyHC isoform mRNAs during postnatal development in mi/mi mice using real-time PCR. By 8 weeks of age, MyHC I had nearly disappeared in the +/+ mice, while it was still present in the mi/mi, and the level of MyHC I mRNA in the mi/mi was 5.1-fold higher than that in the +/+ (p<0.01). The levels of MyHC IIx mRNAs in the mi/mi mice were 41 ~ 55% lower than those in the +/+ at both 3 weeks and 4 weeks of age (p<0.05). No significant difference in the expression of MyHC IIa and IIb mRNAs in the masseter muscle was found between the mi/mi and +/+. From these results, we speculate that the deficiency of teeth affects the masseter muscles during the postnatal development

A short isoform of ATG7 fails to lipidate LC3/GABARAP

Publisher's version (útgefin grein)Autophagy is a degradation pathway important for cellular homeostasis. The E1-like enzyme ATG7 is a key component of the autophagy machinery, with the main function of mediating the lipidation of LC3/GABARAP during autophagosome formation. By analysing mRNA-sequencing data we found that in addition to the full-length ATG7 isoform, various tissues express a shorter isoform lacking an exon of 27 amino acids in the C-terminal part of the protein, termed ATG7(2). We further show that ATG7(2) does not bind LC3B and fails to mediate the lipidation of members of the LC3/GABARAP family. We have thus identified an isoform of ATG7 that is unable to carry out the best characterized function of the protein during the autophagic response. This short isoform will have to be taken into consideration when further studying the role of ATG7.This work was supported by a START Marie Curie/Icelandic Research Fund grant (M.H.O.; grant number 120457-041), Icelandic Research Fund grant (M.H.O.; grant number 184727-051), an Icelandic Cancer Society Research Fund grant (M.H.O.), Icelandic Research Fund grant (E.S.; grant number 152715) and by an Erwin Schrödinger fellowship grant from the Austrian Science Fund (V.F.; grant number: J 3864-B26).Peer Reviewe

Mitf is a master regulator of the v-ATPase, forming a control module for cellular homeostasis with v-ATPase and TORC1

Post-print (lokagerð höfundar)The v-ATPase is a fundamental eukaryotic enzyme that is central to cellular homeostasis. Although its impact on key metabolic regulators such as TORC1 is well documented, our knowledge of mechanisms that regulate v-ATPase activity is limited. Here, we report that the Drosophila transcription factor Mitf is a master regulator of this holoenzyme. Mitf directly controls transcription of all 15 v-ATPase components through M-box cis-sites and this coordinated regulation affects holoenzyme activity in vivo. In addition, through the v-ATPase, Mitf promotes the activity of TORC1, which in turn negatively regulates Mitf. We provide evidence that Mitf, v-ATPase and TORC1 form a negative regulatory loop that maintains each of these important metabolic regulators in relative balance. Interestingly, direct regulation of v-ATPase genes by human MITF also occurs in cells of the melanocytic lineage, showing mechanistic conservation in the regulation of the v-ATPase by MITF family proteins in fly and mammals. Collectively, this evidence points to an ancient module comprising Mitf, v-ATPase and TORC1 that serves as a dynamic modulator of metabolism for cellular homeostasis.This work was supported by the National Institutes of Health, National Eye Institute [grant number R01EY017097 to F.P.]; an RPB Unrestricted Grant and Lions District 20-Y1 award to the Dept. of Ophthalmology, SUNY-UMU (F.P.); the Icelandic Research Fund [grant numbers 130230-053 and 152715-051 to E.S.] a PHC Jules Verne 2014 grant [grant number 31891VM to E.S. and L.L.]; a grant from the Ligue Nationale Contre le Cancer (Equipe labellisee), INCa, Canceropole, Ile de France and Labex CelTisPhyBio [grant number ANR-11-LBX-0038 to L.L.]; and the Ludwig Institute for Cancer Research and the Harry J Lloyd Trust (to C.G.).Peer Reviewe

TFEB regulates murine liver cell fate during development and regeneration

It is well established that pluripotent stem cells in fetal and postnatal liver (LPCs) can differentiate into both hepatocytes and cholangiocytes. However, the signaling pathways implicated in the differentiation of LPCs are still incompletely understood. Transcription Factor EB (TFEB), a master regulator of lysosomal biogenesis and autophagy, is known to be involved in osteoblast and myeloid differentiation, but its role in lineage commitment in the liver has not been investigated. Here we show that during development and upon regeneration TFEB drives the differentiation status of murine LPCs into the progenitor/cholangiocyte lineage while inhibiting hepatocyte differentiation. Genetic interaction studies show that Sox9, a marker of precursor and biliary cells, is a direct transcriptional target of TFEB and a primary mediator of its effects on liver cell fate. In summary, our findings identify an unexplored pathway that controls liver cell lineage commitment and whose dysregulation may play a role in biliary cancer

C-KIT Signaling Depends on Microphthalmia-Associated Transcription Factor for Effects on Cell Proliferation

The development of melanocytes is regulated by the tyrosine kinase receptor c-KIT and the basic-helix-loop-helix-leucine zipper transcription factor Mitf. These essential melanocyte survival regulators are also well known oncogenic factors in malignant melanoma. Despite their importance, not much is known about the regulatory mechanisms and signaling pathways involved. In this study, we therefore sought to identify the signaling pathways and mechanisms involved in c-KIT mediated regulation of Mitf. We report that c-KIT stimulation leads to the activation of Mitf specifically through the c-KIT phosphorylation sites Y721 (PI3 kinase binding site), Y568 and Y570 (Src binding site). Our study not only confirms the involvement of Ras-Erk signaling pathway in the activation of Mitf, but also establishes that Src kinase binding to Y568 and Y570 of c-KIT is required. Using specific inhibitors we observe and verify that c-KIT induced activation of Mitf is dependent on PI3-, Akt-, Src-, p38- or Mek kinases. Moreover, the proliferative effect of c-KIT is dependent on Mitf in HEK293T cells. In contrast, c-KIT Y568F and Y721F mutants are less effective in driving cell proliferation, compared to wild type c-KIT. Our results reveal novel mechanisms by which c-KIT signaling regulates Mitf, with implications for understanding both melanocyte development and melanoma

The spatial scale of competition from recruits on an older cohort in Atlantic salmon

Competitive effects of younger cohorts on older ones are frequently assumed to be negligible in species where older, larger individuals dominate in pairwise behavioural interactions. Here, we provide field estimates of such competition by recruits on an older age class in Atlantic salmon (Salmo salar), a species where observational studies have documented strong body size advantages which should favour older individuals in direct interactions. By creating realistic levels of spatial variation in the density of underyearling (YOY) recruits over a 1-km stretch of a stream, and obtaining accurate measurements of individual growth rates of overyearlings (parr) from capture–mark–recapture data on a fine spatial scale, we demonstrate that high YOY density can substantially decrease parr growth. Models integrating multiple spatial scales indicated that parr were influenced by YOY density within 16 m. The preferred model suggested parr daily mass increase to be reduced by 39% when increasing YOY density from 0.0 to 1.0 m−2, which is well within the range of naturally occurring densities. Reduced juvenile growth rates will in general be expected to reduce juvenile survival (via increased length of exposure to freshwater mortality) and increase generation times (via increased age at seaward migrations). Thus, increased recruitment can significantly affect the performance of older cohorts, with important implications for population dynamics. Our results highlight that, even for the wide range of organisms that rely on defendable resources, the direction of competition among age classes cannot be assumed a priori or be inferred from behavioural observations alone