Spermatozoa represent the morphologically most diverse type of animal cells and show remarkable variation in size across and also within species. To understand the evolution of this diversity, it is important to reveal to what degree this variation is genetic or environmental in origin and whether this depends on species' life histories. Here we applied quantitative genetic methods to a pedigreed multigenerational data set of the collared flycatcher Ficedula albicollis, a passerine bird with high levels of extra-pair paternity, to partition genetic and environmental sources of phenotypic variation in sperm dimensions for the first time in a natural population. Narrow-sense heritability (h2 ) of total sperm length amounted to 0.44 ± 0.14 SE, whereas the corresponding figure for evolvability (estimated as coefficient of additive genetic variation, CVa ) was 0.02 ± 0.003 SE. We also found an increase in total sperm length within individual males between the arrival and nestling period. This seasonal variation may reflect constraints in the production of fully elongated spermatozoa shortly after arrival at the breeding grounds. There was no evidence of an effect of male age on sperm dimensions. In many previous studies on laboratory populations of several insect, mammal and avian species, heritabilities of sperm morphology were higher, whereas evolvabilities were similar. Explanations for the differences in heritability may include variation in the environment (laboratory vs. wild), intensity of sexual selection via sperm competition (high vs. low) and genetic architecture that involves unusual linkage disequilibrium coupled with overdominance in one of the studied species.
- MeSH
- Biological Evolution MeSH
- Phenotype * MeSH
- Quantitative Trait, Heritable * MeSH
- Passeriformes genetics MeSH
- Spermatozoa cytology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
The loss of control of cell proliferation, apoptosis regulation and contact inhibition leads to tumor development. While benign tumors are restricted to their primary space, i.e. where these tumors first originate, the metastatic tumors not only disseminate- facilitated by hypoxia-driven neovascularization- to distant secondary sites but also show substantial changes in metabolism, tissue architectures, gene expression profiles and immune phenotypes. All these alterations result in radio-, chemo- and immune-resistance rendering these metastatic tumor cells refractory to therapy. Since the beginning of the transformation, these factors- which influence each other- are incorporated to the developing and metastasizing tumor. As a result, the complexities in the heterogeneity of tumor progressively increase. This space-time function in the heterogeneity of tumors is generated by various conditions and factors at the genetic as well as microenvironmental levels, for example, endogenous retroviruses, methylation and epigenetic dysregulation that may be etiology-specific, cancer associated inflammation, remodeling of the extracellular matrix and mesenchymal cell shifted functions. On the one hand, these factors may cause de-differentiation of the tumor cells leading to cancer stem cells that contribute to radio-, chemo- and immune-resistance and recurrence of tumors. On the other hand, they may also enhance the heterogeneity under specific microenvironment-driven proliferation. In this editorial, we intend to underline the importance of heterogeneity in cancer progress, its evaluation and its use in correlation with the tumor evolution in a specific patient as a field of research for achieving precise patient-tailored treatments and amelioration of diagnostic (monitoring) tools and prognostic capacity.
- MeSH
- Extracellular Matrix MeSH
- Humans MeSH
- Neoplastic Stem Cells MeSH
- Tumor Microenvironment genetics MeSH
- Neoplasms * genetics MeSH
- Neovascularization, Pathologic MeSH
- Cell Proliferation genetics MeSH
- Check Tag
- Humans MeSH
- Publication type
- Editorial MeSH
... -- Vnitrodruhová disparita 78 -- BOX: Vavilovovy řady a reevoluce znaků 83 -- Část II: Evoluce evolvability ... ... 85 -- 2.1 Podmínky biologické evoluce 87 -- 2.2 Evolvabilita a její historie 91 -- BOX: Novinky na poli ... ... evoluční biologie 93 -- 2.3 Evoluce evolvability 100 -- 2.3.1 Mechanismy evolvability 102 -- 2.3.2 Příčiny ... ... evoluce evolvability 106 BOX: Robustnost 110 -- 2.3.3 Evoluční omezení a jejich role v evoluci 116 - ... ... - BOX: Evolvabilita jako biosémiotická vlastnost 119 -- 2.4 Modularita v biologii 127 -- 2.4.1 Definice ...
Galileo ; svazek 72
Vydání první 311 stran : ilustrace ; 20 cm
Publikace se zabývá několika zásadními otázkami současné evoluční biologie. Určeno odborné veřejnosti.; Monografie přístupnou formou pojednává o několika zásadních otázkách moderní evoluční biologie. Soustředí se zejména na problematiku evolvability a dokládá, že evoluci podléhá i samotná schopnost se vyvíjet. Jak si přitom všímá „tuzemská“ teorie zamrzlé evoluce, evoluci evolvability ovlivňuje řada zajímavých procesů zahrnujících mimo jiné hromadění dále neproměnlivých prvků. Právě nejednoznačná povaha těchto procesů může být vysvětlením (ne)samozřejmého faktu, že se na Zemi setkáváme s tak různorodými produkty biologické evoluce.
- Conspectus
- Obecná genetika. Obecná cytogenetika. Evoluce
- NML Fields
- přírodní vědy
The extrinsic PsbU and PsbV proteins are known to play a critical role in stabilizing the Mn4CaO5 cluster of the PSII oxygen-evolving complex (OEC). However, most isolates of the marine cyanobacterium Prochlorococcus naturally miss these proteins, even though they have kept the main OEC protein, PsbO. A structural homology model of the PSII of such a natural deletion mutant strain (P. marinus MED4) did not reveal any obvious compensation mechanism for this lack. To assess the physiological consequences of this unusual OEC, we compared oxygen evolution between Prochlorococcus strains missing psbU and psbV (PCC 9511 and SS120) and two marine strains possessing these genes (Prochlorococcus sp. MIT9313 and Synechococcus sp. WH7803). While the low light-adapted strain SS120 exhibited the lowest maximal O2 evolution rates (Pmax per divinyl-chlorophyll a, per cell or per photosystem II) of all four strains, the high light-adapted strain PCC 9511 displayed even higher PChlmax and PPSIImax at high irradiance than Synechococcus sp. WH7803. Furthermore, thermoluminescence glow curves did not show any alteration in the B-band shape or peak position that could be related to the lack of these extrinsic proteins. This suggests an efficient functional adaptation of the OEC in these natural deletion mutants, in which PsbO alone is seemingly sufficient to ensure proper oxygen evolution. Our study also showed that Prochlorococcus strains exhibit negative net O2 evolution rates at the low irradiances encountered in minimum oxygen zones, possibly explaining the very low O2 concentrations measured in these environments, where Prochlorococcus is the dominant oxyphototroph.
- MeSH
- Bacterial Proteins chemistry genetics physiology MeSH
- Chlorophyll metabolism MeSH
- Photosynthesis physiology MeSH
- Photosystem II Protein Complex chemistry genetics physiology MeSH
- Genome, Bacterial MeSH
- Oxygen metabolism MeSH
- Models, Molecular MeSH
- Flow Cytometry MeSH
- Cyanobacteria genetics metabolism MeSH
- Light MeSH
- Publication type
- Journal Article MeSH
- Comparative Study MeSH
Robust photosynthesis in chloroplasts and cyanobacteria requires the participation of accessory proteins to facilitate the assembly and maintenance of the photosynthetic apparatus located within the thylakoid membranes. The highly conserved Ycf48 protein acts early in the biogenesis of the oxygen-evolving photosystem II (PSII) complex by binding to newly synthesized precursor D1 subunit and by promoting efficient association with the D2 protein to form a PSII reaction center (PSII RC) assembly intermediate. Ycf48 is also required for efficient replacement of damaged D1 during the repair of PSII. However, the structural features underpinning Ycf48 function remain unclear. Here we show that Ycf48 proteins encoded by the thermophilic cyanobacterium Thermosynechococcus elongatus and the red alga Cyanidioschyzon merolae form seven-bladed beta-propellers with the 19-aa insertion characteristic of eukaryotic Ycf48 located at the junction of blades 3 and 4. Knowledge of these structures has allowed us to identify a conserved "Arg patch" on the surface of Ycf48 that is important for binding of Ycf48 to PSII RCs but also to larger complexes, including trimeric photosystem I (PSI). Reduced accumulation of chlorophyll in the absence of Ycf48 and the association of Ycf48 with PSI provide evidence of a more wide-ranging role for Ycf48 in the biogenesis of the photosynthetic apparatus than previously thought. Copurification of Ycf48 with the cyanobacterial YidC protein insertase supports the involvement of Ycf48 during the cotranslational insertion of chlorophyll-binding apopolypeptides into the membrane.
- MeSH
- Biological Evolution * MeSH
- Behavior physiology classification MeSH
- Physics methods trends MeSH
- Cognitive Science history methods trends MeSH
- Humans MeSH
- Motor Neurons * physiology MeSH
- Reward MeSH
- Pleasure-Pain Principle MeSH
- Prostheses and Implants trends MeSH
- Repression, Psychology MeSH
- Fishes physiology genetics growth & development MeSH
- Consciousness * physiology MeSH
- Visual Perception physiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
The p53 tumor suppressor and its key regulator MDM2 play essential roles in development, ageing, cancer, and cellular stress responses in mammals. Following DNA damage, MDM2 interacts with p53 mRNA in an ATM kinase-dependent fashion and stimulates p53 synthesis, whereas under normal conditions, MDM2 targets the p53 protein for degradation. The peptide- and RNA motifs that interact with MDM2 are encoded by the same conserved BOX-I sequence, but how these interactions have evolved is unknown. Here, we show that a temperature-sensitive structure in the invertebrate Ciona intestinalis (Ci) p53 mRNA controls its interaction with MDM2. We also show that a nonconserved flanking region of Ci-BOX-I domain prevents the p53-MDM2 protein-protein interaction. These results indicate that the temperature-regulated p53 mRNA-MDM2 interaction evolved to become kinase regulated in the mammalian DNA damage response. The data also suggest that the negative regulation of p53 by MDM2 via protein-protein interaction evolved in vertebrates following changes in the BOX-I flanking sequence.
- MeSH
- Apoptosis genetics MeSH
- Ciona intestinalis MeSH
- DNA Primers MeSH
- RNA, Messenger genetics metabolism MeSH
- Cell Line, Tumor MeSH
- Tumor Suppressor Protein p53 genetics metabolism MeSH
- DNA Damage MeSH
- Proto-Oncogene Proteins c-mdm2 genetics metabolism MeSH
- RNA Recognition Motif Proteins genetics metabolism MeSH
- Base Sequence MeSH
- Protein Structure, Tertiary MeSH
- Protein Binding MeSH
- Structure-Activity Relationship MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
Differentiation is a central aspect of the parasite life cycle and encompasses adaptation to both host and environment. If we accept that evolution cannot anticipate an organism's needs as it enters a new environment, how do parasite differentiation pathways arise? The transition between vertebrate and insect stage African trypanosomes is probably one of the better studied and involves a cell-cycle arrested or 'stumpy' form that activates metabolic pathways advantageous to the parasite in the insect host. However, a range of stimuli and stress conditions can trigger similar changes, leading to formation of stumpy-like cellular states. We propose that the origin and optimisation of this differentiation program represents repurposing of a generic stress response to gain considerable gain-of-fitness associated with parasite transmission.
Kazuistika popisuje případ pacientky, u které jsem stanovil postupně diagnózu primární hyperparatyreózy. Pacientka byla nakonec indikována k operačnímu řešení choroby.
A case report is presented of a woman diagnosed with primary hyperparathyreosis. The patient was scheduled for surgery.
- MeSH
- Diagnosis, Differential MeSH
- Hypercalcemia diagnosis etiology MeSH
- Hypertension etiology drug therapy MeSH
- Middle Aged MeSH
- Humans MeSH
- Osteoporosis diagnosis etiology MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Female MeSH
- Publication type
- Case Reports MeSH