The community of root fungi is associated with the growth rate of Norway spruce ( Picea abies )

Our study delved into the relationship between root‐associated fungi, gene expression and plant morphology in Norway spruce cuttings derived from both slow‐and fast‐growing trees. We found no clear link between the gene expression patterns of adventitious roots and the growth phenotype, suggesting no fundamental differences in the receptiveness to fungal symbionts between the phenotypes. Interestingly, saplings from slow‐growing parental trees exhibited a higher richness of ectomycorrhizal species and larger roots. Some ectomycorrhizal species, typically found on mature spruces, were more prevalent on saplings from slow‐growing spruces. The ericoid mycorrhizal fungus, Hyaloscypha hepaticola, showed a stronger association with saplings from fast‐growing spruces. Moreover, saplings from slow‐growing spruces had a greater number of Ascomycete taxa and free‐living saprotrophic fungi. Aboveground sapling stems displayed some phenotypic variation; saplings from fast‐growing phenotypes had longer branches but fewer whorls in their stems compared to those from the slow‐growing group. In conclusion, the observed root‐associated fungi and phenotypic characteristics in young Norway spruces may play a role in their long‐term growth rate. This suggests that the early interactions between spruces and fungi could potentially influence their growth trajectory

Improved chromosome-level genome assembly of the Glanville fritillary butterfly (Melitaea cinxia) integrating Pacific Biosciences long reads and a high-density linkage map

Background The Glanville fritillary (Melitaea cinxia) butterfly is a model system for metapopulation dynamics research in fragmented landscapes. Here, we provide a chromosome-level assembly of the butterfly's genome produced from Pacific Biosciences sequencing of a pool of males, combined with a linkage map from population crosses. Results The final assembly size of 484 Mb is an increase of 94 Mb on the previously published genome. Estimation of the completeness of the genome with BUSCO indicates that the genome contains 92-94% of the BUSCO genes in complete and single copies. We predicted 14,810 genes using the MAKER pipeline and manually curated 1,232 of these gene models. Conclusions The genome and its annotated gene models are a valuable resource for future comparative genomics, molecular biology, transcriptome, and genetics studies on this species.Peer reviewe

The Importance of LDL and Cholesterol Metabolism for Prostate Epithelial Cell Growth

Cholesterol-lowering treatment has been suggested to delay progression of prostate cancer by decreasing serum LDL. We studied in vitro the effect of extracellular LDL-cholesterol on the number of prostate epithelial cells and on the expression of key regulators of cholesterol metabolism. Two normal prostatic epithelial cell lines (P96E, P97E), two in vitro immortalized epithelial cell lines (PWR-1E, RWPE-1) and two cancer cell lines (LNCaP and VCaP) were grown in cholesterol-deficient conditions. Cells were treated with 1–50 µg/ml LDL-cholesterol and/or 100 nM simvastatin for seven days. Cell number relative to control was measured with crystal violet staining. Changes in mRNA and protein expression of key effectors in cholesterol metabolism (HMGCR, LDLR, SREBP2 and ABCA1) were measured with RT-PCR and immunoblotting, respectively. LDL increased the relative cell number of prostate cancer cell lines, but reduced the number of normal epithelial cells at high concentrations. Treatment with cholesterol-lowering simvastatin induced up to 90% reduction in relative cell number of normal cell lines but a 15–20% reduction in relative number of cancer cells, an effect accompanied by sharp upregulation of HMGCR and LDLR. These effects were prevented by LDL. Compared to the normal cells, prostate cancer cells showed high expression of cholesterol-producing HMGCR but failed to express the major cholesterol exporter ABCA1. LDL increased relative cell number of cancer cell lines, and these cells were less vulnerable than normal cells to cholesterol-lowering simvastatin treatment. Our study supports the importance of LDL for prostate cancer cells, and suggests that cholesterol metabolism in prostate cancer has been reprogrammed to increased production in order to support rapid cell growth

Genome sequencing and population genomic analyses provide insights into the adaptive landscape of silver birch

Silver birch (Betula pendula) is a pioneer boreal tree that can be induced to flower within 1 year. Its rapid life cycle, small (440-Mb) genome, and advanced germplasm resources make birch an attractive model for forest biotechnology. We assembled and chromosomally anchored the nuclear genome of an inbred B. pendula individual. Gene duplicates from the paleohexaploid event were enriched for transcriptional regulation, whereas tandem duplicates were overrepresented by environmental responses. Population resequencing of 80 individuals showed effective population size crashes at major points of climatic upheaval. Selective sweeps were enriched among polyploid duplicates encoding key developmental and physiological triggering functions, suggesting that local adaptation has tuned the timing of and cross-talk between fundamental plant processes. Variation around the tightly-linked light response genes PHYC and FRS10 correlated with latitude and longitude and temperature, and with precipitation for PHYC. Similar associations characterized the growth-promoting cytokinin response regulator ARR1, and the wood development genes KAK and MED5A.Peer reviewe

Author Correction: Genome sequencing and population genomic analyses provide insights into the adaptive landscape of silver birch.

In the version of this article initially published, there was a mistake in the calculation of the nucleotide mutation rate per site per generation: 1 × 10−9 mutations per site per generation was used, whereas 9.5 × 10−9 was correct. This error affects the interpretation of population-size changes over time and their possible correspondence with known geological events, as shown in the original Fig. 4 and supporting discussion in the text, as well as details in the Supplementary Note. Neither the data themselves nor any other results are affected. Figure 4 has been revised accordingly. Images of the original and corrected figure panels are shown in the correction notice

Kansalliset kaupunkipuistot Suomessa

Opinnäytetyössä selvitetään, mikä on kansallinen kaupunkipuisto, miten sen idea on tullut Suomeen ja miten se vaikuttaa kaupunkeihin, joihin se on perustettu Suomessa. Työssä käydään läpi kansallisen kaupunkipuiston perustamisedellytyksiä, miten sitä käsitellään maankäyttö- ja rakennuslaissa, mikä sen suhde on kaavoitukseen ja ympäristöministeriön roolia perustamisprosessissa. Opinnäytetyössä käydään läpi nykyisiä ja vireillä olevia kansallisia kaupunkipuistoja. Kansallinen kaupunkipuisto on Ruotsista Suomeen rantautunut idea yhtenäisestä ja laajasta puistoalueesta, joka liittyy olennaisesti kaupungin ydinkeskustaan ja johon kuuluu kaupunkiluonnon monimuotoisuuden säilyttämisen kannalta tärkeitä luonnonalueita. Sen tulee olla riittävän laaja ja eheä. Niitä on Suomessa kahdeksan kappaletta ja lisää on vireillä. Kansallisen kaupunkipuiston statuksen saannista päättää ympäristöministeriö kaupungin hakemuksesta. Tutkimusmenetelmänä käytettiin tiedon tutkintaa ja havainnointia. Tutkimusmateriaalina käytimme internetistä ja kirjoista löytyviä materiaaleja. Pääosa tiedostamme tuli kaupunkien omilta internetsivuilta ja kaupunkien julkaisemista tiedotteista. Suomessa on nykyisiä ja vireillä olevia kansallisia kaupunkipuistoja huomattavasti enemmän, kuin lain muodostumisen aikaan oli suunniteltu. Kansallisten kaupunkipuistojen tuomat hyödyt on todettu erittäin positiivisiksi.The objectives of this thesis were to explain what national urban parks are, how their idea came to Finland and how they affect the cities in which they were established. The purpose was to discuss the national urban park establishment conditions, how they are discussed in the Land Use and Building Act, their relationship to the role of town planning and the role of the Ministry of the Environment in their establishment. this thesis discussed the current and pending national urban parks. The thought of the national urban parks arrived to Finland from Sweden. It is an idea of a uniformed and large park area, which is intrinsically linked to the city center and which includes the maintenance of the important natural areas in urban biodiversity. It should be intact and wide-reaching enough. There are eight national urban parks in Finland and more are pending. For a city to establish a national urban park, the city officials must send an application to the Ministry of Environment and they decide the outcome. The research methods used were examination of data and observation. The material consisted of Internet sources and literature about the subject. The number of the current and pending national urban parks in Finland is considerably higher than it was planned when the legislation was enacted. The benefits of the national urban parks have been deemed very positive

Geenien Ilmenemisen ja Kasvun Säätely Hormonaaliselle Hoidolle Resistentissä Rintasyövässä

Hormonaaliselle hoidolle vastustuskykyisen rintasyövän soluviljelymallit Rintasyöpä on naisten yleisin syöpä. Vuosittain suomessa todetaan 4000–5000 uutta rintasyöpätapausta. Rintasyövistä noin 70 % on hormonireseptoripositiivisia eli niissä ilmenee estrogeenireseptori. Estrogeeni, joka vaikuttaa estrogeenireseptorin kautta, on hormonireseptoripositiivisen, eli hormoniherkän rintasyövän tärkein tunnettu kasvuvaikuttaja. Hormoniherkässä rintasyövässä hormonaaliset hoidot (antiestrogeenit) tähtäävätkin estrogeenin kasvuvaikutuksen estämiseen. Hormonaaliset hoidot ovat tehokkaita hoitomuotoja, sekä liitännäishoitoina annettuna leikkauksen jälkeen, että levinneen rintasyövän hoidossa. Kuitenkin osalla hormonireseptoripositiivisista potilaista ei todeta vastetta hoidolle eli syöpäkasvain on vastustuskykyinen hormonaalisille hoidoille, ja osalla potilaista rintasyöpä uusiutuu sellaisena että se ei enää reagoi annettuun hormonaaliseen hoitoon, eli syöpä on kehittynyt vastustuskykyiseksi (resistenssi) hoidon aikana. Resistenssin syntymekanismeista on saatu tietoa tutkimalla kasvaimista otettuja kudosnäytteitä, sekä laboratoriossa tehtävien soluviljelykokeiden avulla. Tutkimuksessa selvitettiin soluviljelymallien avulla geenien ilmenemisen muutoksia prosessissa, jossa hormoniherkästä rintasyövästä kehittyy resistentti antiestrogeenihoidolle (toremifeeni), ja kun hormoniherkkä rintasyöpä alkaa kasvaa ilman estrogeenia. Tutkimus osoitti että rintasyöpäsolujen pitkäaikaisen lääkealtistuksen (1 vuosi) jälkeen havaitut muutokset geenien ilmenemisessä voidaan nähdä soluissa heti kun ne alkavat kasvaa ilman estrogeenia tai antiestrogeenista huolimatta, jo noin 2-3 kuukauden jälkeen. Tulokset tukevat näkemystä että osalla soluista on valmiiksi kyky kasvaa muuttuneissa olosuhteissa ja ne valikoituvat (selektio) kasvamaan tässä prosessissa. Tutkimuksessa osoitettiin myös että fos-like antigen 1 (FOSL1) geenin yli-ilmentyminen on tärkeä ominaisuus toremifeeni-resistenttien solujen kasvulle. Lisäksi havaittiin, että selektiota ei tapahdu vain resistenssin syntymisen alkuvaiheessa, sillä toremifeeni alkoi vaikuttaa joidenkin geenien säätelyyn vasta pidemmän altistuksen (1 vuosi) jälkeen. Estrogeenin kasvuvaikutuksen estämiseen tähtäävät hoitomuodot tehoavat hormoniherkkään rintasyöpään vaihtelevasti ja hoidoille resistenttien syöpien kehittyminen on yleistä. Tämän takia myös muiden hormonaalisten hoitomuotojen tutkiminen resistenteillä syöpäsoluilla on tärkeää. Tutkimuksessa havaittiin että fysiologisena konsentraationa A-vitamiini hidasti resistenttien rintasyöpäsolujensolujen kasvua, etenkin annettuna yhdessä estrogeenin kanssa. Havaittiin myös että synteettinen progestiini (medroksiprogesteroni asetaatti) jo matalina farmakologisina konsentraatioina esti estrogeenista riippumattomien solujen kasvua, mutta estrogeeni poisti tämän vaikutuksen. Nämä tulokset herättävät mielenkiintoa muista hormonaalisista hoidoista antiestrogeenihoitojen lisänä.Breast cancer is the most common type of cancer among women in western world. In Finnish women, approximately 4000 – 5000 new breast cancers are diagnosed every year. Approximately 70 percent of breast cancers express estrogen receptor (ER). These tumors use estrogen as their main growth stimulus and they are considered to be hormone-dependent. Endocrine therapy targeting ER is the most effective treatment of hormone-dependent breast cancer therapy both in the adjuvant and metastatic setting. In premenopausal women, the main source of estrogen is the ovaries, while in postmenopausal women, the enzyme aromatase converts estrogen from androgens in peripheral tissues such as adipose, skin or bone. In hormone-dependent breast cancer, the suppression of tumor growth can be achieved by reducing estrogen levels with chemical ovarian ablation (occasionally with surgery or radiation) in premenopausal women, or with aromatase inhibitors in postmenopausal women. Also, the interaction of estrogen and ER can be blocked by using selective ER modulators (SERMs) or by downregulating the expression of ER with selective ER downregulators (SERDs) both in premenopausal and postmenopausal women. Endocrine therapy is the most effective treatment for the hormone receptor-positive breast cancer. Still, not all patients receiving endocrine therapy respond to treatment (de novo resistance), and others will eventually relapse despite an initial response (acquired resistance). Knowledge of resistance mechanisms originates mainly from tumor biopsies of tamoxifen-resistant breast cancer, and from in vitro cell culture models of antiestrogen resistance. Several different mechanisms have been hypothesized to be involved in de novo or acquired resistance to endocrine therapy. These mechanisms include the activation of growth factor receptors and their downstream signaling pathways, which lead to an increased estrogen-sensitivity of ER or ligand-independent activation of ER. Such mechanisms may lead breast cancer cells from an estrogen-dependent phenotype which responds to endocrine therapy, to a non-responding estrogen-independent phenotype. This study was undertaken in order to examine the alterations in gene expression when hormone-dependent breast cancer cells were grown over a long-term period without estrogen, or additionally in the presence of the SERM toremifene, eventually leading to estrogen-independent (which mimics resistance to aromatase inhibitor) and toremifene-resistant phenotypes. Our results show that observed alterations in gene expression after long-term culture of the cells were already present as soon as the cells started proliferating after a period of quiescence. This indicates that pre-existing resistant subpopulations were selected, without involving any changes in individual cells. The overexpression of the fos-like antigen 1 (FOSL1) was shown to be critical for the growth of toremifene-resistant cells. We also observed changes in the regulation of genes by toremifene, which took place later in the cell culture process, indicating that the resistant cells acquired a toremifene-stimulated phenotype. This may not have happened in the early selection process. There has been renewed interest in alternative hormonal treatments both in early disease and in the advanced setting when conventional ER-targeting therapies fail. We assessed the effect of different nuclear receptor ligands on the growth of hormone-sensitive breast cancer cells and endocrine-resistant sublines. In our study, physiological concentrations of vitamin A (retinol) inhibited the growth of cell lines, especially in the presence of estrogen. This is interesting since low-dose estrogen therapy is a promising new approach in treating estrogen-independent and antiestrogen-resistant hormone receptor-positive breast cancer. Another intriguing finding was that medroxyprogesterone acetate dose-dependently and at low pharmacological concentrations inhibited the growth of estrogen-independent cells, and that the presence of estrogen abrogated the effect. These findings warrant further study on the effects of combined low-dose estrogen and retinoids, and aromatase inhibitor and synthetic progestins on acquired aromatase inhibitor-resistant breast cancer

Kiinteistönmuodostuksen tilanne ja konsultoinnin näkymät Suomessa

Insinöörityön tarkoituksena oli selvittää, mikä on julkisen kiinteistönmuodostustoiminnan tilanne Suomessa ja voidaanko sitä edistää konsultoinnin avulla. Kiinteistönmuodostus Suomessa on ollut pitkään viranomaistoimintaa, ja se on pääosin hoidettu julkisrahoitteisesti sekä julkisten viranhaltijoiden toimesta. Julkisen sektorin resurssien, kuten taloudellisten ja henkilöresurssien vähentymisen johdosta tilanteeseen tarvitaan ratkaisuja. Julkisen talouden haasteiden lisääntyessä on paineita löytää aiemmista toimintamalleista poikkeavia ratkaisuja. Tutkimuksessa hyödynnettiin kuntakentän kiinteistönmuodostustoimijoille tehtyä kyselyä, jonka tarkoitus oli kerryttää empiirisiä havaintoja aiheesta. Kyselyn tuloksista ilmeni, että resurssitilanne vaihteli kunnittain. Tilanne koettiin joko hyvänä, kohtuullisena tai haastavana. Tilanteen haastavuuteen vaikutti se, oliko kunta joutunut rekrytoimaan uutta työvoimaa ja miten siinä oli onnistuttu. Keskeinen tekijä oli ammattitaito sekä suorat työaikaresurssit. Tärkeimpinä konsultin käytön mahdollisuuksia rajoittavina tekijöinä nähtiin tiukka lainsäädäntö sekä merkittäviltä osin se, ettei maanmittausalalle ole muodostunut käytäntöjä konsultin käytöstä. Konsultin käyttö nähtiin kuitenkin tarkoituksenmukaisena valmistelutyössä, uusien työntekijöiden kouluttamisessa ja kiinteistönmuodostuksen asiakkaan tukena. Kaiken kaikkiaan tulosten perusteella näyttää siltä, että kunnat joutuvat pohtimaan uusia tapoja toteuttaa kiinteistönmuodostusta

Adaptive and non-adaptive gene expression responses in prostate cancer during androgen deprivation.

Androgen deprivation therapy is the cornerstone treatment of advanced prostate cancer. Eventually prostate cancer cells overcome androgen deprivation therapy, giving rise to castration resistant prostate cancer (CRPC) characterized by increased androgen receptor (AR) activity. Understanding the cellular mechanisms leading to CRPC is needed for development of novel treatments. We used long-term cell cultures to model CRPC; a testosterone-dependent cell line (VCaP-T) and cell line adapted to grow in low testosterone (VCaP-CT). These were used to uncover persistent and adaptive responses to testosterone level. RNA was sequenced to study AR-regulated genes. Expression level changed due to testosterone depletion in 418 genes in VCaP-T (AR-associated genes). To evaluate significance for CRPC growth, we compared which of them were adaptive i.e., restored expression level in VCaP-CT. Adaptive genes were enriched to steroid metabolism, immune response and lipid metabolism. The Cancer Genome Atlas Prostate Adenocarcinoma data were used to assess the association with cancer aggressiveness and progression-free survival. Expressions of 47 AR-associated or association gaining genes were statistically significant markers for progression-free survival. These included genes related to immune response, adhesion and transport. Taken together, we identified and clinically validated multiple genes being linked with progression of prostate cancer and propose several novel risk genes. Possible use as biomarkers or therapeutic targets should be studied further