Browsing by Subject "ROLES"

Sort by: Order: Results:

Now showing items 21-24 of 24
  • Wang, Qing-Wei; Robson, Thomas Matthew; Pieristè, Marta; Oguro, Michi; Oguchi, Riichi; Murai, Yoshinori; Kurokawa, Hiroko (2020)
    Although sunlight is essential for plant growth and development, the relative importance of each spectral region in shaping functional traits is poorly understood, particularly in dynamic light environments such as forest ecosystems. We examined responses of 25 functional traits from groups of 11 shade-intolerant and 12 understorey shade-tolerant forb species grown outdoors under five filter treatments differing in spectral transmittance: (a) transmitting c. 95% of solar radiation (280-800 nm); (b) attenuating ultraviolet-B (UV-B); (c) attenuating all UV; (d) attenuating all UV and blue light; (e) attenuating all UV, blue and green light. Our results show that UV-B radiation mainly affected the biochemical traits but blue light mainly affected the physiological traits irrespective of functional strategy, whereas green light affected both sets of traits. This would suggest that differentiation among suites of functional trait responses proceeds according to light quality. Biomass accumulation was significantly increased by UV-A radiation (contrasting treatment [b] vs. [c]) among shade-intolerant but decreased by blue light among shade-tolerant species; green and red light affected whole-plant morphological development differently according to functional groups. Shade-tolerant species were more plastic than shade-intolerant species in response to each spectral region that we examined except for UV-B radiation. Synthesis. Our results show that differences in the spectral composition of sunlight can drive functional trait expression irrespective of total irradiance received. The different responses of functional traits between functional groups imply that shade-tolerant and intolerant species have adapted to utilize spectral cues differently in their respective light environments.
  • Bæk, Kristoffer T.; Bowman, Lisa; Millership, Charlotte; Søgaard, Mia Dupont; Kaever, Volkhard; Siljamäki, Pia Maria; Savijoki, Kirsi Kristiina; Varmanen, Pekka Kristian; Nyman, Tuula Anneli; Gründling, Angelika; Frees, Dorte (2016)
    Lipoteichoic acid (LTA) is an important cell wall component of Gram-positive bacteria and a promising target for the development of vaccines and antimicrobial compounds against Staphylococcus aureus. Here we demonstrate that mutations in the conditionally essential ltaS (LTA synthase) gene arise spontaneously in an S. aureus mutant lacking the ClpX chaperone. A wide variety of ltaS mutations were selected, and among these, a substantial portion resulted in premature stop codons and other changes predicted to abolish LtaS synthesis. Consistent with this assumption, the clpX ltaS double mutants did not produce LTA, and genetic analyses confirmed that LTA becomes nonessential in the absence of the ClpX chaperone. In fact, inactivation of ltaS alleviated the severe growth defect conferred by the clpX deletion. Microscopic analyses showed that the absence of ClpX partly alleviates the septum placement defects of an LTA-depleted strain, while other phenotypes typical of LTA-negative S. aureus mutants, including increased cell size and decreased autolytic activity, are retained. In conclusion, our results indicate that LTA has an essential role in septum placement that can be bypassed by inactivating the ClpX chaperone. IMPORTANCE Lipoteichoic acid is an essential component of the Staphylococcus aureus cell envelope and an attractive target for the development of vaccines and antimicrobials directed against antibiotic-resistant Gram-positive bacteria such as methicillin-resistant S. aureus and vancomycin-resistant enterococci. In this study, we showed that the lipoteichoic acid polymer is essential for growth of S. aureus only as long as the ClpX chaperone is present in the cell. Our results indicate that lipoteichoic acid and ClpX play opposite roles in a pathway that controls two key cell division processes in S. aureus, namely, septum formation and autolytic activity. The discovery of a novel functional connection in the genetic network that controls cell division in S. aureus may expand the repertoire of possible strategies to identify compounds or compound combinations that kill antibiotic-resistant S. aureus.
  • Paavola, Jere; Alakoski, Tarja; Ulvila, Johanna; Kilpiö, Teemu; Sirén, Juuso; Perttunen, Sanni; Narumanchi, Suneeta; Wang, Hong; Lin, Ruizhu; Porvari, Katja; Junttila, Juhani; Huikuri, Heikki; Immonen, Katariina; Lakkisto, Päivi; Magga, Johanna; Tikkanen, Ilkka; Kerkelä, Risto (2020)
    Background Vascular endothelial zinc finger 1 (Vezf1) is a transcription factor previously shown to regulate vasculogenesis and angiogenesis. We aimed to investigate the role of Vezf1 in the postnatal heart. Methods The role of Vezf1 in regulating cardiac growth and contractile function was studied in zebrafish and in primary cardiomyocytes. Findings We find that expression of Vezf1 is decreased in diseased human myocardium and mouse hearts. Our experimental data shows that knockdown of zebrafish Vezf1 reduces cardiac growth and results in impaired ventricular contractile response to β-adrenergic stimuli. However, Vezf1 knockdown is not associated with dysregulation of cardiomyocyte Ca2+ transient kinetics. Gene ontology enrichment analysis indicates that Vezf1 regulates cardiac muscle contraction and dilated cardiomyopathy related genes and we identify cardiomyocyte Myh7/β-MHC as key target for Vezf1. We further identify a key role for an MCAT binding site in the Myh7 promoter regulating the response to Vezf1 knockdown and show that TEAD-1 is a binding partner of Vezf1. Interpretation We demonstrate a role for Vezf1 in regulation of compensatory cardiac growth and cardiomyocyte contractile function, which may be relevant in human cardiac disease.
  • Lundberg, Rickard; Melen, Krister; Westenius, Veera; Jiang, Miao; Österlund, Pamela; Khan, Hira; Vapalahti, Olli; Julkunen, Ilkka; Kakkola, Laura (2019)
    The Zika virus (ZIKV) is a member of the Flaviviridae family and an important human pathogen. Most pathogenic viruses encode proteins that interfere with the activation of host innate immune responses. Like other flaviviruses, ZIKV interferes with the expression of interferon (IFN) genes and inhibits IFN-induced antiviral responses. ZIKV infects through epithelial barriers where IFN-lambda 1 is an important antiviral molecule. In this study, we analyzed the effects of ZIKV proteins on the activation of IFN-lambda 1 promoter. All ZIKV proteins were cloned and transiently expressed. ZIKV NS5, but no other ZIKV protein, was able to interfere with the RIG-I signaling pathway. This inhibition took place upstream of interferon regulatory factor 3 (IRF3) resulting in reduced phosphorylation of IRF3 and reduced activation of IFN-lambda 1 promoter. Furthermore, we showed that ZIKV NS5 interacts with the protein kinase IKK epsilon, which is likely critical to the observed inhibition of phosphorylation of IRF3.