Literatura académica sobre el tema "Concomitant morphogenesis"

Mitotic spindle orientation (SO) is a conserved mechanism that governs cell fate and tissue morphogenesis. In the developing epidermis, a balance between self-renewing symmetric divisions and differentiative asymmetric divisions is necessary for normal development. While the cellular machinery that executes SO is well characterized, the extrinsic cues that guide it are poorly understood. Here, we identified the basal cell adhesion molecule (BCAM), a β1 integrin coreceptor, as a novel regulator of epidermal morphogenesis. In utero RNAi-mediated depletion of Bcam in the mouse embryo did not hinder β1 integrin distribution or cell adhesion and polarity. However, Bcam depletion promoted apoptosis, thinning of the epidermis, and symmetric cell division, and the defects were reversed by concomitant overexpression of the apoptosis inhibitor Xiap. Moreover, in mosaic epidermis, depletion of Bcam or Xiap induced symmetric divisions in neighboring wild-type cells. These results identify apoptosis and epidermal architecture as extrinsic cues that guide SO in the developing epidermis.

Deletion of integrin-β1 ( Itgb1) in the kidney collecting system led to progressive renal dysfunction and polyuria. The defect in the concentrating ability of the kidney was concomitant with decreased medullary collecting duct expression of aquaporin-2 and arginine vasopressin receptor 2, while histological examination revealed hypoplastic renal medullary collecting ducts characterized by increased apoptosis, ectasia and cyst formation. In addition, a range of defects from small kidneys with cysts and dilated tubules to bilateral renal agenesis was observed. This was likely due to altered growth and branching morphogenesis of the ureteric bud (the progenitor tissue of the renal collecting system), despite the apparent ability of the ureteric bud-derived cells to induce differentiation of the metanephric mesenchyme. These data not only support a role for Itgb1 in the development of the renal collecting system but also raise the possibility that Itgb1 links morphogenesis to terminal differentiation and ultimately collecting duct function and/or maintenance.

Although iterative development can be uncoupled from morphogenesis in plant organs, the relationship between the cell cycle and developmental events is not well established in embryos. Zygotes of fucoid algae, including Fucus and Pelvetia are particularly well suited for studying the interaction(s) between cell cycle progression and the early morphogenetic events, as the establishment of polarity and its morphogenetic expression, i.e. germination, and the first cell cycle are concomitant. We have previously demonstrated that, in Fucus zygotes, various aspects of cell cycle progression are tightly controlled by cyclin-dependent kinase (CDK)-like proteins, including two PSTAIRE CDK-like proteins, p34 and p32, which are synthesised after fertilisation. We show that specific inhibition of CDK-like proteins, either with purine derivatives such as olomoucine and amino-purvalanol or by microinjection of the CDK inhibitor p21cip1, prevents germination and cell division. Whereas direct inhibition of DNA replication by aphidicolin did not affect polarised development, olomoucine, which has previously been shown to prevent entry in S phase, and other purine derivatives also inhibited photopolarisation. Early microinjection of a monoclonal anti-PSTAIRE antibody also prevented germination and cell division. Only p34 had affinity for amino-purvalanol, suggesting that among PSTAIRE CDKs, this protein is the main target of purine derivatives. Models to account for the simultaneous control of early cell cycle progression and polarisation are proposed.

Neutral lipids, predominantly triacylglycerol (TAG) and sterol ester, are stored within the cellular organelles termed lipid droplets (LDs). Although it is believed that the major function of LDs is to supply the cell with energy and membranes, little is known about the cellular events directly involving LDs and their contents. In this study, we provide cytological evidence that LDs form direct contacts with the prospore membrane (PSM) that is synthesized de novo during meiosis II to sequester the dividing nuclei in sporulating yeast. Lipidomic analyses indicate that TAG lipolysis releases free fatty acids at a time that correlates well with meiosis II progression, concomitant with phospholipid remodeling. Mutants lacking TAG or impaired of TAG hydrolysis show spore wall assembly defects, supporting a role for TAG and/or its metabolites in spore wall morphogenesis. Not only does LD integrity influence spore wall assembly, LDs are also essential for other aspects of spore development. Yeast cells lacking LDs are severely defective in PSM growth and organization and display disrupted spindles, producing dead spores or even failing to form spores. Together these results link LD physiology directly to a unique membrane morphogenesis process critical for development.

Explants of cucumber seedlings having different lengths of hypocotyl attached were grown axenically on Murashige and Skoog medium supplemented with kinetin (2 mg L-1). Multiple shoots developed from the apical regions of all explants. In this tissue shoots may also develop at the base of the hypocotyl, but this response is strongly dependent upon the length of the hypocotyl. As the length of the hypocotyl increased beyond 5 mm, there was a rapid reduction in basal shoot numbers and a concomitant increase in root production. We suggest that these responses are related not to the ratio or concentration of endogenous growth regulators but to different regions of sensitivity to growth regulators along the hypocotyl.

Anticlinal ordinary epidermal cell wall waviness is a widespread feature found in the leaves of a variety of land plant species. However, it has not yet been encountered in leaves with multiple epidermides. Surprisingly, in Magnolia grandiflora leaves, ordinary epidermal cells in both layers of the bi-layered adaxial epidermis exhibit wavy anticlinal contour. During the development of the above cells, cortical microtubules are organized in anticlinally oriented bundles under the anticlinal walls, and radial arrays extending from the bundles at the edges of anticlinal and external periclinal walls, under the external periclinal walls. This microtubule pattern is followed by cell wall reinforcement with local thickenings, the cellulose microfibrils of which are parallel to the underlying microtubules. This specialized microtubule organization and concomitant cell wall reinforcement is initiated in the external epidermal layer, while hypodermis follows. The waviness pattern of each epidermal layer is unrelated to that of the other. The above findings are discussed in terms of morphogenetic mechanism induction and any implications in the functional significance of ordinary epidermal cell waviness.

Apoptosis plays important roles in various stages of organogenesis. In this study, we hypothesized that apoptosis would play an important role in tooth morphogenesis. We examined the role of apoptosis in early tooth development by using a caspase inhibitor, z-VAD-fmk, concomitant with in vitro organ culture and tooth germ transplantation into the kidney capsule. Inhibition of apoptosis at the early cap stage did not disrupt the cell proliferation level when compared with controls. However, the macroscopic morphology of mice molar teeth exhibited dramatic alterations after the inhibition of apoptosis. Crown height was reduced, and mesiodistal diameter was increased in a concentration-dependent manner with z-VAD-fmk treatment. Overall, apoptosis in the enamel knot would be necessary for the proper formation of molar teeth, including appropriate shape and size.

The aim of the study was to identify the features of the clinical course and morphogenesis of infective endocarditis (IE) in HIVinfected injecting drug users with concomitant hepatitis C virus infection in comparison with the clinical and morphological picture of endocarditis in persons without drug dependence. It was found that the causative agent of IE in HIV-infected patients was staphylococcus aureus (71.8%), and in persons without drug dependence in the etiology of the disease the conditionally pathogenic flora prevailed. In HIV-infected drug-dependent patients, the tricuspid valve was affected (82.7%), and in persons without drug dependence — isolated aortic valve damage (40%) and combined mitral and aorticvalve lesions (36.4%). Purulent sepsis complications in drug-dependent patients with IE are less common than in patients without drug dependence due to immunosuppression, which is present in HIV-infected persons.

While evidence on the impact of the biomechanical environment elasticity on human mesenchymal stem cell (hMSC) behavior is growing, the aspect of micropatterning is still poorly understood. Thus, the present study aimed at investigating the influence of defined environmental micropatterning on hMSC behavior. Following characterization, hMSCs were grown on defined pillar micropatterns of 5, 7, 9, and 11 μm. With respect to cell behavior, primary hMSC adhesion was detected by indirect immunofluorescence (iIF) for paxillin, vinculin, integrin αV, and actin, while proliferation was visualized by histone H3. Morphogenesis was monitored by scanning electron microscopy and the expression of stem cell-specific biomarkers by real-time PCR. Favoritism of primary adhesion of hMSCs on pillar tops occurred at smaller pillar micropatterns, concomitant with cell flattening. While vinculin, integrin αV, and paxillin appeared initially more cytoplasmic, high pillar micropatterns favored a progressive redistribution with polarization to cell tension sites and at cell borders. Accomplishment of morphogenesis at day 3 revealed establishment of fully rotund cell somata at 5 μm, while hMSCs appeared progressively elongated at rising micropatterns. The hMSC proliferation capacity was influenced by pillar micropatterns and gene expression analysis of stem cell- and differentiation-associated biomarkers disclosed clear modulation by distinct pillar micropatterns. In response to environmental biomechanics, our results show that hMSC behavior is governed by pillar micropatterning. In turn, these findings may form the basis to prospectively direct lineage specificity of hMSCs in a customized fashion.

Trichomonas vaginalis is a prevalent causative agent that causes trichomoniasis leading to uropathogenic inflammation in the host. The crucial role of the actin cytoskeleton in T. vaginalis cytoadherence has been established but the associated signaling has not been fully elucidated. The present study revealed that the T. vaginalis second messenger PIP2 is located in the recurrent flagellum of the less adherent isolate and is more abundant around the cell membrane of the adherent isolates. The T. vaginalis phosphatidylinositol-4-phosphate 5-kinase (TvPI4P5K) with conserved activity phosphorylating PI(4)P to PI(4, 5)P2 was highly expressed in the adherent isolate and partially colocalized with PIP2 on the plasma membrane but with discrete punctate signals in the cytoplasm. Plasma membrane PIP2 degradation by phospholipase C (PLC)-dependent pathway concomitant with increasing intracellular calcium during flagellate-amoeboid morphogenesis. This could be inhibited by Edelfosine or BAPTA simultaneously repressing parasite actin assembly, morphogenesis, and cytoadherence with inhibitory effects similar to the iron-depleted parasite, supporting the significance of PIP2 and iron in T. vaginalis colonization. Intriguingly, iron is required for the optimal expression and cell membrane trafficking of TvPI4P5K for in situ PIP2 production, which was diminished in the iron-depleted parasites. TvPI4P5K-mediated PIP2 signaling may coordinate with iron to modulate T. vaginalis contact-dependent cytolysis to influence host cell viability. These observations provide novel insights into T. vaginalis cytopathogenesis during the host-parasite interaction.

La morphogenèse est le processus de remodelage du zygote, la cellule œuf fécondée, qui permet d’obtenir la forme finale de l’animal. Chez l’embryon, les combinaisons de profils d’expression génique déterminent les axes de symétrie du corps et établissent les coordonnées spatiotemporelles de spécification des cellules. Ces profils affectent aussi l’organisation des composants du cytosquelette pour réguler la morphogenèse des tissus. Tandis qu’un travail important a été réalisé pour comprendre comment les motifs d’expression génique antéro-postérieur (AP) et dorso-ventral (DV) contrôlent indépendamment la morphogenèse, on en sait toujours peu sur l’impact du croisement de ces motifs. Nous utilisons l’embryon de drosophile comme modèle et nous concentrons sur le processus de repliement tissulaire, un processus vital pour l’animal. Des anomalies de repliement peuvent en effet altérer la neurulation chez les vertébrés et la gastrulation chez l’ensemble des animaux organisés en trois feuillets primordiaux. Les études passées ont montré qu’un réseau d’actomyosine, couvrant la surface médiale-apicale des futures cellules mésodermiques, et sous le contrôle du motif d’expression génique DV, joue un rôle clé dans l’invagination du mésoderme. Néanmoins, les preuves expérimentales et théoriques ont plaidé contre la constriction apicale comme seul mécanisme responsable de l’invagination. Dans cette étude, j’ai mis à jour un réseau jonctionnel sous contrôle des profils d’expression génique AP et DV. Ce réseau contractile génère une tension le long de l’axe apico-basal des cellules et dans le plan du tissu, initiant l’intercalation des cellules à 10-15 μm à l’intérieur de l’épithélium mésodermique. Les forces latérales dans les cellules mésodermiques semblent jouer un rôle à la fois dans l’extension du mésoderme et dans l’invagination. Pour conclure, à travers l’implémentation de microscopie à feuillet de lumière 4D, d’ablation infrarouge femtoseconde pour perturber le cytosquelette et d’optogénétique pour contrôler synthétiquement la morphologie tissulaire, ce travail montre sous un jour nouveau l’origine et les fonctions d’un mécanisme inédit responsable de l’élongation et du repliement coordonnés du tissu
Morphogenesis is the process of reshaping single-cell zygotes to the final form of a developed animal. Embryonic gene patterning systems determine the body axes and lay down the spatiotemporal specification coordinates for cells. Gene patterning systems also affect the organization of cytoskeletal components in order to drive tissue morphogenesis. While much work was done to understand how AP and DV patterning independently control morphogenesis, little is known on how cross-patterning functions. We use the Drosophila embryo as a model system and focus on the process of tissue folding, a process that is vital for the animal since folding defects can impair neurulation in vertebrates and gastrulation in all animals which are organized into the three germ layers. Past work has shown that an actomyosin meshwork spanning the apical-medial side of prospective mesoderm cells and under the control of the embryo DV patterning plays a key role in mesoderm invagination. Nevertheless, both experimental and theoretical pieces of evidence have argued against apical constriction being the sole mechanism driving invagination. In this study, I have uncovered a lateral cell junctional network under the control of both AP and DV patterning. This contractile network generates tension along the apical-basal axis and within the tissue plane, 10-15 μm inside the mesoderm epithelium initiating lateral cell intercalation. Lateral forces in mesoderm cells seem to play a multivalent role in both driving mesoderm extension and invagination. Finally, by implementing 4D multi-view light-sheet imaging, infra-red femtosecond ablation to perturb the cytoskeleton, and optogenetics to synthetically control tissue morphology, this work shines new light on the origin and functions of a novel mechanism responsible for coordinated tissue elongation and folding

Dextral looping is a complex process which progresses concomitantly with cardiac chamber differentiation and ultimately leads to the final alignment of the cardiac regions. Generation of cardiac asymmetry is crucial to ensure the proper form and consequent function of the heart and thus is a highly regulated process. Molecular signals originate long before morphological asymmetry and therefore can direct it; a complex regulatory network has been characterized which invariably converges on the Tgf-β‎ signalling molecule Nodal and its downstream target, the homeobox transcription factor Pitx2. We review current data regarding the cellular and molecular bases of cardiac looping and laterality, and describe current understaning of the role of Nodal and Pitx2. The morphogenetic role of the Pitx2 gene and its modulation of transcription and function, which have recently linked laterality to atrial fibrillation, are emphasized.

Abstract Cell adhesion assays are most often carried out on rigid planar substrata coated with ligands that facilitate cell binding and cell spreading. These ligands include: complex extracellular matrices (ECM; i.e. basement membrane), defined extra cellular matrix proteins (i.e. laminin), short peptide fragments of ECM proteins that bind integrins (i.e. contain RGD sequences) or antibodies that engage, and in some cases cluster, cell surface integrins. Under these conditions integrin dependent signalling events and changes to the cytoskeleton can be assessed, often concomitantly. These classical ‘stick-and-spread’ assays have proven particularly useful for identifying the mechanisms responsible for basic adhesion dependent phenotypes such as anchorage-dependent proliferation, membrane ruffling, or the initiation of cell motility (1-3). However, it is rarely technically possible to examine more complex differentiative phenotypes using these assays. For example, mammary epithelial cells spread on a rigid basement membrane substratum and begin to proliferate. In contrast, when these cells are placed on a malleable gel of the same matrix, morphogenesis and differentiation occur. Given the complexity inherent in the emergence of the latter phenotypes it is very difficult to determine the molecular mediators responsible. To overcome this problem we have developed specialized assays in which the entire process can be deconstructed such that individual morphogenic and differentiative events can be assayed and manipulated in isolation (4-6).