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PubMed2006

Quantitative contributions of blue light and PAR to the photocontrol of plant morphogenesis in Trifolium repens (L.).

Shade-avoidance is a major adaptive response of plants, and is usually considered to be controlled by phytochromes through the perception of changes in the red:far red light ratio. However, few studies on the effects of blue light (BL) and of light intensity [photosynthetically active radiation (PAR)] on light-grown plants have been conducted, especially concerning changes in PAR at constant BL. The objective here was to quantify the photocontrol of aerial morphogenesis by BL and PAR. Experiments were conducted varying BL and PAR independently, with three BL levels (4, 38, and 83 micromol m(-2) s(-1)) at constant PAR (300 micromol m(-2) s(-1)) and three PAR levels (338, 705, and 163 micromol m(-2) s(-1)) at constant BL (36 micromol m(-2) s(-1)). Effects on morphogenetic processes were analysed as quantitative modulations of ontogenic trends and response curves were produced. White clover (Trifolium repens L.) was used, as it is a typical shade-avoider displaying the whole syndrome of shade-avoidance in a purely vegetative stage. Morphological responses were strongly controlled by both BL and PAR changes, through antagonist effects on leaf appearance rate and additive effects on petiole elongation. All the other responses appeared to be the indirect consequences of changes in the leaf appearance rates. BL acted as a light signal for plant morphogenesis. However, the PAR control probably implicates two distinct mechanisms, such as a trophic effect and a signal. Both PAR and BL actions involved organ-specific differences, which are central in the control of the shade-avoidance responses.

Color↗

PubMed2006

Genetic interaction between the AS1-AS2 and RDR6-SGS3-AGO7 pathways for leaf morphogenesis.

In higher plants, class I KNOTTED1-like homeobox (KNOX) gene suppression and leaf polarity establishment are two processes crucial for leaf morphogenesis. The Arabidopsis genes, ASYMMETRIC LEAVES1 and 2 (AS1 and AS2), are required for repressing the class I KNOX genes and promoting leaf adaxial cell fates. In addition, the RNA-DEPENDENT RNA POLYMERASE6 (RDR6) gene acts synergistically with AS1 and AS2 to specify the adaxial polarity and repress the KNOX genes in leaves. It is known that RDR6 is one of the key components in plant post-transcriptional gene silencing (PTGS), and is likely to function with other silencing components in a genetic pathway in regulating leaf patterning. Here we report phenotypic analyses of double mutants combining as1 or as2 with other mutations relating to different RNA silencing pathways. We show that plants carrying rdr6, suppressor of gene silencing3 (sgs3) or zippy (zip, also called ago7) in combination with as1 or as2 demonstrate severe morphological defects, and the double mutant plants are generally similar to one another. Detailed phenotypic and molecular analyses reveal that leaves of rdr6 as2(1), sgs3 as2(1) and zip as2(1) all show an abnormal adaxial identity, and contain high levels of microRNA165/166 and FILAMENTOUS FLOWER (FIL) transcripts. These results suggest that RDR6, SGS3 and AGO7 act in the same pathway, which genetically interacts with the AS1-AS2 pathway for leaf development. The RDR6-SGS3-AGO7 pathway was previously identified as regulating the plant vegetative phase change. Our results reveal a new function of the pathway, which is also required for normal leaf morphogenesis.

Arabidopsis↗

PubMed2003

Ovarian regulation of endometrial gland morphogenesis and activin-follistatin system in the neonatal ovine uterus.

Postnatal development of the ovine uterus between birth and Postnatal Day (PND) 56 involves differentiation of the endometrial glandular epithelium from the luminal epithelium followed by tubulogenesis and branching morphogenesis. Previous results indicated that ovariectomy of ewes at birth did not affect uterine growth or initial stages of endometrial gland genesis on PND 14 but did affect uterine growth after PND 28. Available evidence from a number of species supports the hypothesis that the ovary does not affect endometrial gland morphogenesis in the postnatal uterus. To test this hypothesis in our sheep model, ewes were assigned at birth to a sham surgery as a control or bilateral ovariectomy (OVX) on PND 7. Uteri were removed and weighed on PND 56. Ovariectomy did not affect circulating levels of estradiol-17beta. Uterine weight was 52% lower in OVX ewes. Histomorphological analyses indicated that the thickness of the endometrium and myometrium, total number of endometrial glands, and endometrial gland density in the stratum spongiosum stroma was reduced in uteri of OVX ewes. In contrast, the number of superficial ductal gland invaginations and gland density in the stratum compactum stroma was not affected by ovariectomy. The uteri of OVX ewes contained lower levels of betaA subunit, activin receptor (ActR) type IA, ActRIB, and follistatin protein expression but higher levels of betaB subunit. In the neonatal ovary, follistatin, inhibin alpha subunit, betaA subunit, and betaB subunit were expressed in antral follicles between PNDs 0 and 56. These results led to rejection of the hypothesis that the ovary does not influence endometrial adenogenesis. Rather, the ovary and, thus, an ovarian-derived factor regulates, in part, the coiling and branching morphogenetic stage of endometrial gland development after PND 14 and expression of specific components of the activin-follistatin system in the neonatal ovine uterus that appear to be important for that critical process.

Activin Receptors↗

PubMed2006

Vascular endothelial growth factor and kinase domain region receptor are involved in both seminiferous cord formation and vascular development during testis morphogenesis in the rat.

Morphological male sex determination is dependent on migration of endothelial and preperitubular cells from the adjacent mesonephros into the developing testis. Our hypothesis is that VEGFA and its receptor KDR are necessary for both testicular cord formation and neovascularization. The Vegfa gene has 8 exons with many splice variants. Vegfa120, Vegfa164, and Vegfa188 mRNA isoforms were detected on Embryonic Day (E) 13.5 (plug date=E0) in the rat. Vegfa120, Vegfa144, Vegfa164, Vegfa188, and Vegfa205 mRNA were detected at E18 and Postnatal Day 3 (P3). Kdr mRNA was present on E13.5, whereas Fms-like tyrosine kinase 1 receptor (Flt1) mRNA was not detected until E18. VEGFA protein was localized to Sertoli cells at cord formation and KDR to germ and interstitial cells. The VEGFA signaling inhibitors SU1498 (40 microM) and VEGFR-TKI (8 microM) inhibited cord formation in E13 testis cultures with 90% reduced vascular density (P<0.01) in VEGFR-TKI-treated organs. Furthermore, Je-11 (10 microM), an antagonist to VEGFA, also perturbed cord formation and inhibited vascular density by more than 50% (P<0.01). To determine signal transduction pathways involved in VEGFA's regulation of testis morphogenesis, E13 testis were treated with LY 294002 (15 microM), a phosphoinositide 3-kinase (PI3K) pathway inhibitor, resulting in inhibition of both vascular density (46%) and cord formation. Thus, we support our hypothesis and conclude that VEGFA, secreted by the Sertoli cell, is involved in both neovascularization and cord formation and potentially acts through the PI3K pathway during testis morphogenesis to elicit its effects.

Animals↗

PubMed1990

Membrane morphogenesis from cloned fragments of bacteriophage PM2 DNA that contain the sp6.6 gene.

The formation of new membrane vesicles normally occurs during eukaryotic organellogenesis and maturation of bacteriophage PM2. This virus was studied as a simple model for membrane morphogenesis. Previous biochemical and genetic studies suggest that a major structural protein of PM2, sp6.6, is an integral membrane protein involved in viral membrane morphogenesis. To establish the necessity of sp6.6 in membrane formation, restriction fragments of PM2 that contained the sp6.6 coding sequence were cloned into several plasmid vectors for expression in Escherichia coli. A construction in pBR322 containing two HindIII fragments of PM2 DNA caused production of intracellular membrane vesicles of the same size as those produced in the course of natural infection of Alteromonas espejiana. Similar results were obtained with a smaller construct of HindIII fragments in the plasmid vector pPL-lambda. Expression of sp6.6 was detected via incorporation of 35S-labeled methionine after SDS-polyacrylamide gel electrophoresis and with a specific rabbit antiserum on immunoblots. Other constructs did not produce recognizable vesicles or sp6.6. These results are the first to suggest that a hydrophobic membrane protein can cause development of new membrane structure.

Bacteriophages↗

PubMed2004

Transgenic expression of mammalian heparanase uncovers physiological functions of heparan sulfate in tissue morphogenesis, vascularization, and feeding behavior.

We have generated homozygous transgenic mice (hpa-tg) overexpressing human heparanase (endo-beta-D-glucuronidase) in all tissues and characterized the involvement of the enzyme in tissue morphogenesis, vascularization, and energy metabolism. Biochemical analysis of heparan sulfate (HS) isolated from newborn mice and adult tissues revealed a profound decrease in the size of HS chains derived from hpa-tg vs. control mice. Despite this, the mice appeared normal, were fertile, and exhibited a normal life span. A significant increase in the number of implanted embryos was noted in the hpa-tg vs. control mice. Overexpression of heparanase resulted in increased levels of urinary protein and creatinine, suggesting an effect on kidney function, reflected also by electron microscopy examination of the kidney tissue. The hpa-tg mice exhibited a reduced food consumption and body weight compared with control mice. The effect of heparanase on tissue remodeling and morphogenesis was best demonstrated by the phenotype of the hpa-tg mammary glands, showing excess branching and widening of ducts associated with enhanced neovascularization and disruption of the epithelial basement membrane. The hpa-tg mice exhibited an accelerated rate of hair growth, correlated with high expression of heparanase in hair follicle keratinocytes and increased vascularization. Altogether, characterization of the hpa-tg mice emphasizes the involvement of heparanase and HS in processes such as embryonic implantation, food consumption, tissue remodeling, and vascularization.

Animals↗

PubMed1997

Inhibition of prostate ductal morphogenesis by retinoic acid.

PURPOSE: To examine the effect of retinoic acid on prostate ductal morphogenesis. MATERIALS AND METHODS: Newborn male Balb/C mice were injected with 25 mg./kg. all-trans retinoic acid or vehicle alone. Animals were sacrificed at 60 days of age and prostate ductal morphology was quantitatively assessed by microdissection. Total prostate DNA was quantitated by DPA assay. RESULTS: The greatest effect was seen in the ventral prostate. Retinoic acid treated animals showed a 20% decrease in mean number of branch-points (p = 0.0006) with a corresponding 13% decrease in duct tips (p = 0.026). The combined ventral and dorsal prostate showed an effect with a 12% decrease in ductal branchpoints (p = 0.048). There was no effect on animal or organ weight and no effect on DNA content within the prostate. There was no difference in the prostate histology of treated and control animals. CONCLUSION: Retinoic acid administration in the newborn period inhibits mouse prostate ductal morphogenesis. This effect appears independent of an inhibition of overall growth.

Animals↗

PubMed2004

Notch signaling in vascular morphogenesis.

PURPOSE OF REVIEW: This review highlights recent developments in the role of the Notch signaling pathway during vascular morphogenesis, angiogenesis, and vessel homeostasis. RECENT FINDINGS: Studies conducted over the past 4 years have significantly advanced the understanding of the effect of Notch signaling on vascular development. Major breakthroughs have elucidated the role of Notch in arterial versus venular specification and have placed this pathway downstream of vascular endothelial growth factor. SUMMARY: An emerging hallmark of the Notch signaling pathway is its nearly ubiquitous participation in cell fate decisions that affect several tissues, including epithelial, neuronal, hematopoietic, and muscle. The vascular compartment has been the latest addition to the list of tissues known to be regulated by Notch. Unraveling the contribution of Notch signaling to blood vessel formation has resulted principally from gain-of-function and loss-of-function experiments in mouse and zebrafish. During the past 4 years, these mechanistic studies have revealed that Notch is required for the successful completion of several steps during vascular morphogenesis and differentiation. In addition, the findings that Notch mutations are linked to some late-onset hereditary vascular pathologic conditions suggest the added contribution of this signaling pathway to vascular homeostasis.

Animals↗

PubMed2000

New concepts in fission yeast morphogenesis.

The ability to generate spatial form is a fundamental characteristic of all living organisms, which has been much studied by successive generations of developmental biologists. In recent years increasing numbers of cell biologists have turned their attention to the mechanisms by which cells generate their spatial form. These include the mechanisms that position components in different places within the cell, that specify the position of these components, and that generate the overall shape of these components. These problems are entirely analogous to those studied by developmental biologists, although usually at the level of the whole organism, organ or tissue. Because the organization of all cells is basically similar, it is possible that the concepts and the underlying molecular mechanisms of cell morphogenesis may be highly conserved. In this article we consider the generation of spatial form within the fission yeast cell, focusing on emerging new concepts, which may be applicable to the morphogenesis of other cells.

Morphogenesis↗

PubMed2000

Trichome morphogenesis in Arabidopsis.

Trichomes (plant hairs) in Arabidopsis thaliana are large non-secreting epidermal cells with a characteristic three-dimensional architecture. Because trichomes are easily accessible to a combination of genetic, cell biological and molecular methods they have become an ideal model system to study various aspects of plant cell morphogenesis. In this review we will summarize recent progress in the understanding of trichome morphogenesis.

Arabidopsis↗

PubMed1979

Morphology and morphogenesis of a new paramyxovirus (PMV 107).

The morphology of the virions and nucleocapsids of paramyxovirus 107 (PVM 107) and the replication of the virus were investigated by electron microscopy. The virions and nucleocapsids exhibited the same structural properties as other paramyxoviruses. Nuclecapsids were found in the nucleus and cytoplasm of infected bovine embryonic lung (BEL) cell cultures. A similar situation has been described for the morbilliviruses measles, SSPE, distemper and rinderpest. Alignment of nucleocapsids beneath the plasma membrane and budding of PMV 107 in the productive BEL cell infections were also similar to the morbillivirus-infected cells. In a line of monkey cells (CV1) persistently infected with PMV 107 only cytoplasmic nucleocapsids could be demonstrated. On the basis of its morphology and morphogenesis it is suggested that PMV 107 should be classified as a paramyxovirus. Since nucleocapsids could also be found in the nucleus of infected BEL cells the morphogenesis of PMV 107 closely resembles that of viruses of the morbillivirus group.

Animals↗

PubMed1979

Morphogenesis of nuclear inclusions and virus capsids in HEL cells infected with temperature-sensitive mutants of human cytomegalovirus.

The morphogenesis of nuclear inclusions and virus capsids in human embryonic lung cells infected with ts mutants of human cytomegalovirus at permissive (34 degrees C) and non-permissive (39 degrees C) temperatures was studied by indirect immunofluorescence (IF) and electron microscopic analyses and compared with the morphogenesis of these structures in wild-type virus infection with or without phosphonoacetate. Mutants tested belonged to five different complementation groups: two groups were DNA- (those unable to synthesize virus DNA at 39 degrees C) and the others were dna+. Based on the previous finding that the electron-dense, reticular nuclear inclusions (EM-NI) observed by the thin-section analysis correspond with nuclear inclusions (IF-NI) detected by the indirect IF staining (i.e. they occupy the same space in the nucleus), the following conclusions were obtained in ts mutant infection at 39 degrees C: (i) the formation of EM-NI, IF-NI and virus capsids requires replication of virus DNA. (II) The formation of EM-NI is not necessarily accompanied by the formation of IF-NI; EM-NI itself is not IF-positive unless it acquires virus-specific late antigens. (iii) The assembly of virus capsids occurs only in those cells in which EM-NI is formed; however, it can occur without the formation of IF-NI. (iv) Virus capsids assembled are not the major antigens responsible for the fluorescence of nuclear inclusions.

Capsid↗

PubMed1980

Colony morphology, ultrastructure and morphogenesis in Mycoplasma hominis, Acholeplasma laidlawii and Ureaplasma urealyticum.

Colonies of Mycoplasma hominis, Acholeplasma laidlawii (three strains) and Ureaplasma urealyticum were examined by light and electron microscopy and their characteristic morphology, ultrastructure and morphogenesis are described. Mycoplasma hominis and A. laidlawii, PG8 and oral strains, developed typical 'fried-egg' colonies which were remarkably heterogeneous in size. The colonies of A. laidlawii strain NCTC 10116 were more homogeneous and grew mainly on the surface of the agar showing a fine granular appearance. Ureaplasma urealyticum produced smaller, granular colonies which grew deeply embedded in the agar and generally without much surface growth. The cellular ultrastructure in these colonies was also examined. The results indicate that several aspects of colony morphogenesis and ultrastructure varied for each of the three species examined.

Acholeplasma laidlawii↗

PubMed1992

The effect of AMP on the NAD-dependent glutamate dehydrogenase during activation and morphogenesis in the cellular slime moulds.

In extracts from vegetative Dictyostelium discoideum V12 the basal NAD-dependent glutamate dehydrogenase (NAD-GDH) activity was low, but it increased on standing at 4 degrees C. When 0.1 mM-AMP was included in the assay mix, enzyme activity was stimulated nearly 30-fold. As the extract was allowed to age, the enzyme rapidly lost its ability to be stimulated by AMP. The response of NAD-GDH to AMP was also dependent on the stage of morphogenesis. The ratios of NAD-GDH activity assayed with and without AMP (+AMP/-AMP ratios) in freshly prepared extracts from cells at 0, 4, 8 and 12 h of development were similar, but declined later in morphogenesis. The +AMP/-AMP ratio decreased sharply during activation at 4 degrees C in extracts from cells at 0, 4, 16 and 20 h of development. By contrast, extracts from cells starved for 8 and 12 h remained more responsive to AMP throughout activation. Analysis of Western blots showed that vegetative NAD-GDH did not undergo any detectable proteolytic cleavage during 96 h of activation at 4 degrees C. Also, no change in molecular mass appeared to take place within the cells until culmination (20-24 h), when some breakdown products appeared. Activation of NAD-GDH also occurred in D. discoideum strains NC4 and AX3, and in D. mucoroides. In addition, the enzyme from these four strains was stimulated by AMP and the +AMP/-AMP ratio declined with similar kinetics during activation. The enzyme from Polysphondylium violaceum was not activated on standing, but it was stimulated by AMP. The effect of activation of NAD-GDH is discussed in relation to a postulated catabolic role for this enzyme.

Adenosine Monophosphate↗

PubMed1999

Morphogenesis is coordinated with nuclear division in germinating Aspergillus nidulans conidiospores.

Germinating Aspergillus nidulans conidiospores switch to polarized apical growth following an initial period of isotropic expansion. At the same time, they re-enter the nuclear division cycle. The relationship between spore polarization and nuclear division was investigated by testing the effect of cell cycle inhibitors and temperature-sensitive cell cycle mutations on spore morphogenesis. On rich media, it was found that spore polarization is delayed if completion of the first mitosis is blocked. The observed delay may be dependent upon the activity of the mitosis-promoting NIMA kinase. An additional mechanism appears to prevent polarization as the spore progresses through its first S phase. In contrast, on poor media, spore polarization does not require completion of the first mitosis. These observations suggest that spore morphogenesis is influenced by cell cycle signals in a growth-dependent manner.

Aspergillus nidulans↗

PubMed1999

Inactivation of the KIPMR1 gene of Kluyveromyces lactis results in defective cell-wall morphogenesis.

The P-type Ca2+ -ATPases are the transporters responsible for calcium homeostasis in the cell compartments of eukaryotes. The KIPMR1 gene of Kluyveromyces lactis encodes a P-type Ca2+ -ATPase, which is functionally and structurally homologous to Pmr1p of Saccharomyces cerevisiae, the calcium pump localized in the Golgi membranes. In this work, a novel involvement of KIPmr1p in cell-wall morphogenesis of K. lactis is reported. KIpmr1delta cells exhibited the loss of outer-chain extension in the glycosylation of secreted proteins. The absence of KIPmr1p resulted in the accumulation of round, large cells with an abnormally thick cell wall, as revealed by transmission electron microscopy. The deletant strain also showed a delocalized deposition of chitin in the lateral cell wall accompanied by an unbalanced ratio of insoluble to soluble glucans. These morphological defects were accompanied by the presence of irregularly shaped nuclei and by a DNA content greater than 2n. Addition of 10 mM Ca2+ to the medium of the KIpmr1delta strain reversed the chitin-deposition impairment, recovered the alteration to the glucan ratio and restored a normal thickness of the cell wall. The mutant cells resumed wild-type size, shape and nuclear morphology but the DNA content indicated the persistence of defects in the co-ordination between DNA replication and cell division. The glycosylation defects were completely unaffected by the calcium supplement. These results indicate that calcium homeostasis controlled by KIPmr1p plays an important role in the cell-wall morphogenesis of K. lactis.

Calcium↗

PubMed1996

Essential role of stromal mesenchyme in kidney morphogenesis revealed by targeted disruption of Winged Helix transcription factor BF-2.

Metanephric mesenchyme gives rise to both the epithelial cells of the nephron and the stromal cells of the mature kidney. The function of the stroma. in kidney morphogenesis is poorly understood. We have generated mice with a null mutation in the Winged Helix (WH) transcription factor BF-2 to examine its function during development. BF-2 expression within the developing kidney is restricted to the stromal cell lineage. Homozygotes die within the first 24 hr after birth with abnormal kidneys. Mutant kidneys are small, fused longitudinally, and rotated 90 degrees ventrally. Histological examination reveals a smaller collecting system, numerous large condensations of mesenchyme, and a decrease in the number of nephrons. Using molecular markers we show that induction and condensation of the nephrogenic mesenchyme occurs normally in mutant. The disruption of BF-2 reduces the rate of differentiation of the condensed mesenchyme into tubular epithelium, as well as the rate of growth and branching of the ureter and collecting system. Our findings demonstrate that BF-2 and stromal cells have essential functions during kidney morphogenesis. Furthermore, they suggest that BF-2 controls the production, by the stroma, of signals or factors that are required for the normal transition of induced mesenchyme into tubular epithelium and full growth and branching of the collecting system.

Animals↗

PubMed1997

GATA4 transcription factor is required for ventral morphogenesis and heart tube formation.

Previous studies have suggested that the GATA4 transcription factor plays an important role in regulating mammalian cardiac development. In the studies described in this report we have used gene targeting to produce GATA4-deficient mice. Homozygous GATA4-deficient (GATA4-/-) mice died between 8.5 and 10.5 days post coitum (dpc). GATA4-/- embryos displayed severe defects in both rostral-to-caudal and lateral-to-ventral folding, which were reflected in a generalized disruption of the ventral body pattern. This resulted in the defective formation of an organized foregut and anterior intestinal pore, the failure to close both the amniotic cavity and yolk sac, and the uniform lack of a ventral pericardial cavity and heart tube. Analysis of cardiac development in the GATA4-/- mice demonstrated that these embryos developed splanchnic mesoderm, which differentiated into primitive cardiac myocytes that expressed contractile proteins. However, consistent with the observed defect in ventral morphogenesis, these GATA4-/- procardiomyocytes failed to migrate to the ventral midline to form a linear heart tube and instead formed aberrant cardiac structures in the anterior and dorsolateral regions of the embryo. The defect in ventral migration of the GATA4-/- procardiomyocytes was not cell intrinsic because GATA4-/- cardiac myocytes and endocardial cells populated the hearts of GATA4-/- -C57BL/6 chimeric mice. Taken together, these results demonstrated that GATA4 is not essential for the specification of the cardiac cell lineages. However, they define a critical role for GATA4 in regulating the rostral-to-caudal and lateral-to-ventral folding of the embryo that is needed for normal cardiac morphogenesis.

Animals↗