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Results for “budding”

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PubMed2000

The hormonal regulation of axillary bud growth in Arabidopsis.

Apically derived auxin has long been known to inhibit lateral bud growth, but since it appears not to enter the bud, it has been proposed that its inhibitory effect is mediated by a second messenger. Candidates include the plant hormones ethylene, cytokinin and abscisic acid. We have developed a new assay to study this phenomenon using the model plant Arabidopsis. The assay allows study of the effects of both apical and basal hormone applications on the growth of buds on excised nodal sections. We have shown that apical auxin can inhibit the growth of small buds, but larger buds were found to have lost competence to respond. We have used the assay with nodes from wild-type and hormone-signalling mutants to test the role of ethylene, cytokinin and abscisic acid in bud inhibition by apical auxin. Our data eliminate ethylene as a second messenger for auxin-mediated bud inhibition. Similarly, abscisic acid signalling is not to be required for auxin action, although basally applied abscisic can enhance inhibition by apical auxin and apically applied abscisic acid can reduce it. By contrast, basally applied cytokinin was found to release lateral buds from inhibition by apical auxin, while apically applied cytokinin dramatically increased the duration of inhibition. These results are consistent with cytokinin acting independently to regulate bud growth, rather than as a second messenger for auxin. However, in the absence of cytokinin-signalling mutants, a role for cytokinin as a second messenger for auxin cannot be ruled out.

Abscisic Acid↗

PubMed2002

The roles of bud-site-selection proteins during haploid invasive growth in yeast.

In haploid strains of Saccharomyces cerevisiae, glucose depletion causes invasive growth, a foraging response that requires a change in budding pattern from axial to unipolar-distal. To begin to address how glucose influences budding pattern in the haploid cell, we examined the roles of bud-site-selection proteins in invasive growth. We found that proteins required for bipolar budding in diploid cells were required for haploid invasive growth. In particular, the Bud8p protein, which marks and directs bud emergence to the distal pole of diploid cells, was localized to the distal pole of haploid cells. In response to glucose limitation, Bud8p was required for the localization of the incipient bud site marker Bud2p to the distal pole. Three of the four known proteins required for axial budding, Bud3p, Bud4p, and Axl2p, were expressed and localized appropriately in glucose-limiting conditions. However, a fourth axial budding determinant, Axl1p, was absent in filamentous cells, and its abundance was controlled by glucose availability and the protein kinase Snf1p. In the bud8 mutant in glucose-limiting conditions, apical growth and bud site selection were uncoupled processes. Finally, we report that diploid cells starved for glucose also initiate the filamentous growth response.

Actins↗

PubMed2004

Interactions among Rax1p, Rax2p, Bud8p, and Bud9p in marking cortical sites for bipolar bud-site selection in yeast.

In the budding yeast Saccharomyces cerevisiae, selection of the bud site determines the axis of polarized cell growth and eventual oriented cell division. Bud sites are selected in specific patterns depending on cell type. These patterns appear to depend on distinct types of marker proteins in the cell cortex; in particular, the bipolar budding of diploid cells depends on persistent landmarks at the birth-scar-distal and -proximal poles that involve the proteins Bud8p and Bud9p, respectively. Rax1p and Rax2p also appear to function specifically in bipolar budding, and we report here a further characterization of these proteins and of their interactions with Bud8p and Bud9p. Rax1p and Rax2p both appear to be integral membrane proteins. Although commonly used programs predict different topologies for Rax2p, glycosylation studies indicate that it has a type I orientation, with its long N-terminal domain in the extracytoplasmic space. Analysis of rax1 and rax2 mutant budding patterns indicates that both proteins are involved in selecting bud sites at both the distal and proximal poles of daughter cells as well as near previously used division sites on mother cells. Consistent with this, GFP-tagged Rax1p and Rax2p were both observed at the distal pole as well as at the division site on both mother and daughter cells; localization to the division sites was persistent through multiple cell cycles. Localization of Rax1p and Rax2p was interdependent, and biochemical studies showed that these proteins could be copurified from yeast. Bud8p and Bud9p could also be copurified with Rax1p, and localization studies provided further evidence of interactions. Localization of Rax1p and Rax2p to the bud tip and distal pole depended on Bud8p, and normal localization of Bud8p was partially dependent on Rax1p and Rax2p. Although localization of Rax1p and Rax2p to the division site did not appear to depend on Bud9p, normal localization of Bud9p appeared largely or entirely dependent on Rax1p and Rax2p. Taken together, the results indicate that Rax1p and Rax2p interact closely with each other and with Bud8p and Bud9p in the establishment and/or maintenance of the cortical landmarks for bipolar budding.

Binding Sites↗

PubMed2005

Tumour budding detected by laminin-5 {gamma}2-chain immunohistochemistry is of prognostic value in epidermoid anal cancer.

BACKGROUND: Markers for guidance with regard to individual prognosis and treatment planning are sought in epidermoid anal cancer. This study assessed the prognostic and predictive value of tumour budding. PATIENTS AND METHODS: From a population-based consecutive series of patients who were prospectively recorded, it was possible to investigate 209 (76%) of the pretreatment biopsies. Immunohistochemistry with a monoclonal antibody for the gamma2 chain of laminin-5 was used to detect tumour budding (defined as dissociated single cancer cells or clusters of up to five cells). RESULTS: Tumour budding was detected in 104 (50%) of the 209 samples. No significant correlation was found between tumour budding and clinicopathological characteristics. Patients with tumour budding had a statistically significantly better 5-year overall survival rate compared with patients lacking tumour budding (74% versus 64%, P <0.05). Albeit not statistically significant, other outcome variables such as tumour-specific survival, recurrence after initial complete response and rate of distant metastases, were all in favour of patients with tumour budding. Multivariate analysis reveals tumour budding as an independent positive prognostic factor. CONCLUSIONS: Tumour budding detected by laminin-5 immunohistochemistry may be of prognostic value in the treatment of epidermoid anal cancer. However, further studies are needed to clarify the possible clinical implications.

Adult↗

PubMed2005

Bud morphology and shoot growth dynamics in two species of Mediterranean sub-shrubs co-existing in gypsum outcrops.

BACKGROUND AND AIMS: Understanding the effects of the environment on the morphology and shoot growth activities of plants is crucial to identifying plant ecological strategies. This study analysed the bud morphology, bud activity, shoot growth dynamics and shoot water content at full hydration (WC(h)) of two species of Mediterranean sub-shrubs, Lepidium subulatum and Linum suffruticosum, co-existing in gypsum outcrops in north-east Spain. METHODS: Sampling was conducted monthly over 2 years in one population per species. Buds were dissected under a stereo-microscope. Shoot growth was measured as the mean increase in shoot length of 15 marked individuals between two consecutive samplings. Bud activity was studied following the variations in the number of leaf primordia shorter than 1 mm and longer than 0.025 mm in the buds. KEY RESULTS: Both species bore naked buds and displayed discontinuous seasonal patterns of shoot growth, leaf primordia formation and WC(h). The number of leaf primordia in the bud peaked before the beginning of shoot expansion. In both species, organogenesis and expansion were uncoupled throughout the year. The time lapse between these two processes varied throughout the year, and was greatest for those elements differentiated in autumn. WC(h) was more closely related to shoot expansion than to organogenesis. CONCLUSIONS: Both species displayed similar bud morphology and similar seasonal patterns of bud and shoot growth, and WC(h) as a result of the strong seasonality of the Mediterranean climate in gypsum outcrops. The beginning of the spring period of expansion of long branches coincided with maximum values of WC(h), while the rest period of summer matched minimum values. These results support the hypothesis that the growth of long branches is strongly related to WC(h).

Calcium Sulfate↗

PubMed2006

Physiological changes in gentian axillary buds during two-step preculturing with sucrose that conferred high levels of tolerance to desiccation and cryopreservation.

BACKGROUND AND AIMS: Induction of dehydration tolerance is a key to achieving high survival rates in cryopreservation of plant specimens. It has been reported previously that two-step preculturing with sucrose effectively increased desiccation tolerance in axillary buds of gentian (Gentiana scabra), which allow the buds to survive cryopreservation. This study is aimed at characterizing each step of this preculturing and to elucidate physiological changes induced during this preculturing. METHODS: In standard two-step preculture, excised gentian axillary buds were incubated for 11 d on MS medium with 0.1 m sucrose at 25 degrees C (first step: mild osmotic stress was given) and the subsequent incubation on MS medium with 0.4 m and 0.7 m sucrose for 1 d each (second step). The levels of abscisic acid (ABA), proline and soluble sugars in gentian buds during the preculture were determined. Effects of various combinations of two-step preculturing and of exogenous ABA and proline were studied. KEY RESULTS: During the first preculture step, there was a transient increase in ABA content peaking on day 4, which declined to a background level at the end of the first and second step preculturing. Proline level increased steadily during the first preculture step and increased further in the second preculture step. Incubating buds with medium containing proline, instead of the two-step preculturing, did not allow them to survive desiccation. Incubating buds with ABA instead of 0.1 m sucrose-preculturing effectively increased desiccation tolerance only when it was followed by the second preculture step. Fluridone, an ABA synthesis inhibitor included in the two-step preculture medium, reduced desiccation tolerance of the buds. The normal first-step preculture increased the levels of soluble sugars 2.4-fold, especially sucrose and raffinose. Buds treated with the second preculture step had greatly increased sucrose levels. CONCLUSIONS: These observations lead to the hypothesis that the first preculture step involves ABA-mediated cellular changes and the second step induces loading of sucrose in the gentian buds.

Abscisic Acid↗

PubMed1998

Changes in protein interactions of cell cycle-related genes during the dormancy-to-growth transition in pea axillary buds.

Apical dominance is a phenomenon in which a terminal bud grows predominantly and the growth of the axillary buds is suppressed. Here, we investigated the molecular mechanisms associated with cell cycle control that occur in pea axillary buds as a result of decapitation. Proliferating cell nuclear antigen (PCNA) protein was detected in both dormant and growing buds, while PCNA mRNA was absent in dormant buds. Pissa; CycB1;2 and Cdc2 proteins were undetectable during dormancy. To analyze an interaction between PCNA and Pissa;CycD3;1, we performed anti-PCNA immunoaffinity column chromatography. Pissa;CycD3;1 protein was detected in the eluate prepared from the dormant buds, but not in the eluate prepared from the growing buds. Furthermore, we performed anti-Pissa;CycD3;1 immunoaffinity column chromatography. PCNA protein was detected in the eluate prepared from the dormant buds, but not in the eluate prepared from the growing buds. These results indicated that PCNA associated with Pissa;CycD3;1 only during dormancy. In addition, the interaction between PCNA and Pissa;CycD3;1 was confirmed by a yeast two-hybrid system.

Amino Acid Sequence↗

PubMed1997

Effects of near-lethal heat stress on bud break, heat-shock proteins and ubiquitin in dormant poplar (Populus nigra Charkowiensis x P. nigra incrassata).

We assessed the effects of near-lethal heat stress on bud break, heat-shock proteins (HSPs) and ubiquitin in hybrid poplar (Populus nigra (L.) Charkowiensis x P. nigra (L.) incrassata). Shoots, with 10-15 buds each, were collected from September to March and exposed to temperatures between 20 and 60 degrees C for 2 h. Shoots were then placed in a greenhouse at 18-22 degrees C with supplemental light and cumulative bud break was recorded over a 4-week period. Samples of bud tissues were collected during and up to 96 h after heat treatment for protein analysis. De novo synthesis of proteins was monitored by exposing excised buds to [(35)S]-methionine for 3 h before, during, or after heat treatment. Heat treatments of 40-45 degrees C resulted in both a release from endodormancy and a decrease in thermal units needed for bud break during ecodormancy. The response to near-lethal heat stress was complex and was affected by intrinsic thermal sensitivity. Heat treatments were least effective during August and became progressively more effective as endodormancy progressed. In the later stages of ecodormancy, a heat treatment of 45 degrees C either inhibited bud break or killed the buds. Although temperatures of 42.5 to 45 degrees C inhibited incorporation of [(35)S]-methionine into proteins for at least 48 h, several HSPs were synthesized in response to temperatures of 40-45 degrees C. Immunoblots indicated that one of the heat-induced proteins was immunologically related to HSP70. Increases in free and conjugated forms of ubiquitin were also observed in response to heat treatment. Production of HSPs and ubiquitin, however, was not consistently associated with the heat treatments that induced the highest percentage of bud break. The roles of heat-induced protein degradation, HSPs, and ubiquitin in overcoming dormancy by near-lethal heat stress are discussed.

Journal Article↗

PubMed1998

Effects of elevated CO(2) and temperature on cold hardiness and spring bud burst and growth in Douglas-fir (Pseudotsuga menziesii).

We examined effects of elevated CO(2) and temperature on cold hardiness and bud burst of Douglas-fir (Pseudotsuga menziesii (Mirb.) Franco) seedlings. Two-year-old seedlings were grown for 2.5 years in semi-closed, sunlit chambers at either ambient or elevated (ambient + ~ 4 degrees C) air temperature in the presence of an ambient or elevated (ambient + ~ 200 ppm) CO(2) concentration. The elevated temperature treatment delayed needle cold hardening in the autumn and slowed dehardening in the spring. At maximum hardiness, trees in the elevated temperature treatment were less hardy by about 7 degrees C than trees in the ambient temperature treatment. In general, trees exposed to elevated CO(2) were slightly less hardy during hardening and dehardening than trees exposed to ambient CO(2). For trees in the elevated temperature treatments, date to 30% burst of branch terminal buds was advanced by about 6 and 15 days in the presence of elevated CO(2) and ambient CO(2), respectively. After bud burst started, however, the rate of increase in % bud burst was slower in the elevated temperature treatments than in the ambient temperature treatments. Time of bud burst was more synchronous and bud burst was completed within a shorter period in trees at ambient temperature (with and without elevated CO(2)) than in trees at elevated temperature. Exposure to elevated temperature reduced final % bud burst of both leader and branch terminal buds and reduced growth of the leader shoot. We conclude that climatic warming will influence the physiological processes of dormancy and cold hardiness development in Douglas-fir growing in the relatively mild temperate region of western Oregon, reducing bud burst and shoot growth.

Journal Article↗

PubMed1981

Role of indoleacetic Acid and abscisic Acid in the correlative control by fruits of axillary bud development and leaf senescence.

When fully filled pods of bean plants were deseeded, the rate of axillary bud growth and the chlorophyll content of leaves were increased. Application of 0.1% indoleacetic acid (IAA) in lanolin on the deseeded pods caused abscission of axillary buds, inhibited growth of the remaining buds, and decreased leaf chlorophyll content. The response of bud development to fruit-applied IAA was concentration dependent between 0.001 and 0.1% IAA (representing from 2 to 200 micrograms IAA per fruit) resulting in greater growth inhibition at higher IAA concentrations.When plants were defruited so that the number of fruits per plant was adjusted to 0, 6, 12, or 18, a dosage effect of fruits on photosynthesis was observed. Removal of all fruits caused a rise in the CO(2)-exchange rate (CER). With increasing fruit dosage, plants showed leaf senescence of increasing intensity and a corresponding decline in CER. In contrast to the effect of fruit-applied IAA on leaves and buds, it delayed the senescence of treated fruits. When axillary buds were treated directly with aqueous solutions of IAA, no growth inhibition occurred.Abscisic acid (AbA) applied on deseeded pods, up to a concentration of 0.1% AbA in lanolin, failed to inhibit axillary bud development or to cause leaf senescence.The results support the hypothesis that the correlative control of axillary bud development and leaf senescence by fruits involves the participation of both IAA and AbA. IAA, released by the seeds, may play the role of the correlative signal that moves from the fruit to the target organ, where it stimulates the synthesis or accumulation of AbA. AbA, in turn, may be responsible for the inhibition of axillary bud development and the enhancement of leaf senescence.

Journal Article↗

PubMed1996

FGF induces new feather buds from developing avian skin.

Induction of skin appendages involves a cascade of molecular events. The fibroblast growth factor (FGF) family of peptide growth factors is involved in cell proliferation and morphogenesis. We explored the role of the FGFs during skin appendage induction using developing chicken feather buds as a model. FGF-1, FGF-2, or FGF-4 was added directly to the culture medium or was released from pre-soaked Affigel blue beads. Near the midline, FGFs led to fusion of developing feather buds, representing FGFs' ability to expand feather bud domains in developing skin. In lateral regions of the explant where feather placodes have not formed, FGF treatment produces a zone of condensation and a region with an increased number of feather buds. In ventral epidermis that is normally apteric (without feathers), FGFs can also induce new feather buds. Like normal feather buds, the newly induced buds express Shh. The expression of Grb, Ras, Raf, and Erk, intracellular signaling molecules known to be downstream to tyrosine kinase receptors such as the FGF receptor, was enriched in feather bud domains. Genistein, an inhibitor of tyrosine kinase, suppressed feather bud formation and the effect of FGF. These results indicate that there are varied responses to FGFs depending on epithelial competence. All the phenotypic responses, however, show that FGFs facilitate the formation of skin appendage domains.

Animals↗

PubMed1973

Budding in the dimorphic fungus Phialophora dermatitidis.

Ultrastructural comparisons of yeast and hyphal bud formation in Phialophora dermatitidis reveal that bud initiation is characterized by a blastic rupture of the outer portion of the yeast or hyphal wall and the emergence of a bud protuberance through the resulting opening. The wall of the emerging bud is continuous, with only an inner wall layer of the parental yeast or hypha. The outer, ruptured portion of the parental wall typically forms a collar around the constricted emergence region of the developing bud. The cytoplasm within the very young emerging bud invariably contains a small number of membrane-bound vesicles. The septum formed between the daughter bud and the parental yeast or hypha is a complete septum devoid of a septal pore, septal pore plug, or any associated Woronin bodies characteristic of simple septa of the moniliform or true hyphae. These observations suggest that yeast bud formation and lateral hyphal bud formation in the dimorphic fungus P. dermatitidis involve a growth process which occurs identically in both the yeast and mold phase of this human pathogenic organism.

Cell Wall↗

PubMed2003

Overlapping motifs (PTAP and PPEY) within the Ebola virus VP40 protein function independently as late budding domains: involvement of host proteins TSG101 and VPS-4.

The VP40 protein of Ebola virus can bud from mammalian cells in the form of lipid-bound, virus-like particles (VLPs), and late budding domains (L-domains) are conserved motifs (PTAP, PPxY, or YxxL; where "x" is any amino acid) that facilitate the budding of VP40-containing VLPs. VP40 is unique in that potential overlapping L-domains with the sequences PTAP and PPEY are present at amino acids 7 to 13 of VP40 (PTAPPEY). L-domains are thought to function by interacting with specific cellular proteins, such as the ubiquitin ligase Nedd4, and a component of the vacuolar protein sorting (vps) pathway, tsg101. Mutational analysis of the PTAPPEY sequence of VP40 was performed to understand further the contribution of each individual motif in promoting VP40 budding. In addition, the contribution of tsg101 and a second member of the vps pathway, vps4, in facilitating budding was addressed. Our results indicate that (i) both the PTAP and PPEY motifs contribute to efficient budding of VP40-containing VLPs; (ii) PTAP and PPEY can function as L-domains when separated and moved from the N terminus (amino acid position 7) to the C terminus (amino acid position 316) of full-length VP40; (iii) A VP40-PTAP/tsg101 interaction recruits tsg101 into budding VLPs; (iv) a VP40-PTAP/tsg101 interaction recruits VP40 into lipid raft microdomains; and (v) a dominant-negative mutant of vps4 (E228Q), but not wild-type vps4, significantly inhibited the budding of Ebola virus (Zaire). These results provide important insights into the complex interplay between viral and host proteins during the late stages of Ebola virus budding.

Adenosine Triphosphatases↗

PubMed1996

Genetic analysis of the bipolar pattern of bud site selection in the yeast Saccharomyces cerevisiae.

Previous analysis of the bipolar budding pattern of Saccharomyces cerevisiae has suggested that it depends on persistent positional signals that mark the region of the division site and the tip of the distal pole on a newborn daughter cell, as well as each previous division site on a mother cell. In an attempt to identify genes encoding components of these signals or proteins involved in positioning or responding to them, we identified 11 mutants with defects in bipolar but not in axial budding. Five mutants displaying a bipolar budding-specific randomization of budding pattern had mutations in four previously known genes (BUD2, BUD5, SPA2, and BNI1) and one novel gene (BUD6), respectively. As Bud2p and Bud5p are known to be required for both the axial and bipolar budding patterns, the alleles identified here probably encode proteins that have lost their ability to interact with the bipolar positional signals but have retained their ability to interact with the distinct positional signal used in axial budding. The function of Spa2p is not known, but previous work has shown that its intracellular localization is similar to that postulated for the bipolar positional signals. BNI1 was originally identified on the basis of genetic interaction with CDC12, which encodes one of the neck-filament-associated septin proteins, suggesting that these proteins may be involved in positioning the bipolar signals. One mutant with a heterogeneous budding pattern defines a second novel gene (BUD7). Two mutants budding almost exclusively from the proximal pole carry mutations in a fourth novel gene (BUD9). A bud8 bud9 double mutant also buds almost exclusively from the proximal pole, suggesting that Bud9p is involved in positioning the proximal pole signal rather than being itself a component of this signal.

Cell Polarity↗

PubMed2000

Saccharomyces cerevisiae cdc42p GTPase is involved in preventing the recurrence of bud emergence during the cell cycle.

The Saccharomyces cerevisiae Cdc42p GTPase interacts with multiple regulators and downstream effectors through an approximately 25-amino-acid effector domain. Four effector domain mutations, Y32K, F37A, D38E, and Y40C, were introduced into Cdc42p and characterized for their effects on these interactions. Each mutant protein showed differential interactions with a number of downstream effectors and regulators and various levels of functionality. Specifically, Cdc42(D38E)p showed reduced interactions with the Cla4p p21-activated protein kinase and the Bem3p GTPase-activating protein and cdc42(D38E) was the only mutant allele able to complement the Deltacdc42 null mutant. However, the mutant protein was only partially functional, as indicated by a temperature-dependent multibudded phenotype seen in conjunction with defects in both septin ring localization and activation of the Swe1p-dependent morphogenetic checkpoint. Further analysis of this mutant suggested that the multiple buds emerged consecutively with a premature termination of bud enlargement preceding the appearance of the next bud. Cortical actin, the septin ring, Cla4p-green fluorescent protein (GFP), and GFP-Cdc24p all predominantly localized to one bud at a time per multibudded cell. These data suggest that Cdc42(D38E)p triggers a morphogenetic defect post-bud emergence, leading to cessation of bud growth and reorganization of the budding machinery to another random budding site, indicating that Cdc42p is involved in prevention of the initiation of supernumerary buds during the cell cycle.

Actins↗

PubMed1997

Ureteric bud cells secrete multiple factors, including bFGF, which rescue renal progenitors from apoptosis.

Kidney development requires reciprocal interactions between the ureteric bud and the metanephrogenic mesenchyme. Whereas survival of mesenchyme and development of nephrons from mesenchymal cells depends on signals from the invading ureteric bud, growth of the ureteric bud depends on signals from the mesenchyme. This codependency makes it difficult to identify molecules expressed by the ureteric bud that regulate mesenchymal growth. To determine how the ureteric bud signals the mesenchyme, we previously isolated ureteric bud cell lines (UB cells). These cells secrete soluble factors which rescue the mesenchyme from apoptosis. We now report that four heparin binding factors mediate this growth activity. One of these is basic fibroblast growth factor (bFGF), which is synthesized by the ureteric bud when penetrating the mesenchyme. bFGF rescues three types of progenitors found in the mesenchyme: precursors of tubular epithelia, precursors of capillaries, and cells that regulate growth of the ureteric bud. These data suggest that the ureteric bud regulates the number of epithelia and vascular precursors that generate nephrons by secreting bFGF and other soluble factors.

Animals↗

PubMed2001

Regulation of ureteric bud outgrowth by Pax2-dependent activation of the glial derived neurotrophic factor gene.

The outgrowth of the ureteric bud from the posterior nephric duct epithelium and the subsequent invasion of the bud into the metanephric mesenchyme initiate the process of metanephric, or adult kidney, development. The receptor tyrosine kinase RET and glial cell-derived neurotrophic factor (GDNF) form a signaling complex that is essential for ureteric bud growth and branching morphogenesis of the ureteric bud epithelium. We demonstrate that Pax2 expression in the metanephric mesenchyme is independent of induction by the ureteric bud. Pax2 mutants are deficient in ureteric bud outgrowth and do not express GDNF in the uninduced metanephric mesenchyme. Furthermore, Pax2 mutant mesenchyme is unresponsive to induction by wild-type heterologous inducers. In normal embryos, GDNF is sufficient to induce ectopic ureter buds in the posterior nephric duct, a process inhibited by bone morphogenetic protein 4. However, GDNF replacement in organ culture is not sufficient to stimulate ureteric bud outgrowth from Pax2 mutant nephric ducts, indicating additional defects in the nephric duct epithelium of Pax2 mutants. Pax2 can activate expression of GDNF in cell lines derived from embryonic metanephroi. Furthermore, Pax2 protein can bind to upstream regulatory elements within the GDNF promoter region and can transactivate expression of reporter genes. Thus, activation of GDNF by Pax2 coordinates the position and outgrowth of the ureteric bud such that kidney development can begin.

Animals↗

PubMed2004

In vitro delayed senescence of extirpated buds from zooids of the colonial tunicate Botryllus schlosseri.

In the colonial growth of botryllid ascidians, blastogenesis (bud formation) is a cyclical and synchronized developmental process characterized by a weekly rhythm of budding and apoptotic events. Very little is known about this cycle regulation and its control. In this study, the in vitro fate of developing buds and regressing zooids extirpated from Botryllus schlosseri colonies at different blastogenic stages were examined, revealing that stages 'B' to 'D' buds (but not stage 'A' buds) developed new structures under in vitro conditions. These were mainly spheres (up to 1 mm in diameter) and epithelial monolayers around the attached buds. We also found that: (1) when attached spheres and epithelial monolayers appeared, the life expectancy of an isolated bud in vitro reached 50-60 days, five times the life expectancy of intact, in vivo developing zooids; (2) the life expectancy of in vitro buds that remained unattached to the substrates was at least 150 days; (3) after attaching to the substrates, buds obeyed a newly imposed developmental clock dictating up to 35 survival days for spheres and up to 14 days for epithelial monolayers; (4) the prevailing mode of death in vitro was necrotic, in contrast to the apoptotic mode of zooidal deterioration at the takeover phase of blastogenesis; (5) under in vitro conditions, degenerating zooids surprisingly produced epithelial monolayers within 3 weeks of culturing. Monolayers survived for up to 10 additional days, extending the lifespan of the degenerating zooids from a few hours to up to 1 month. We conclude that under in vitro conditions, not only are the underlying colonial growth mechanisms replaced by different developmental pathways, but also the internal colonial-level clocks programming death, are replaced by a new biological mechanism with different timetables.

Aging↗