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Ralf J Sommer - One of the best experts on this subject based on the ideXlab platform.
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hairy like transcription factors and the evolution of the nematode Vulva equivalence group
Current Biology, 2006Co-Authors: Benjamin Schlager, Waltraud Roseler, Arturo Gutierrez, Min Zheng, Ralf J SommerAbstract:Summary Background Nematode Vulva formation provides a paradigm to study the evolution of pattern formation and cell-fate specification. The Caenorhabditis elegans Vulva is generated from three of six equipotent cells that form the so-called Vulva equivalence group. During evolution, the size of the Vulva equivalence group has changed: Panagrellus redivivus has eight, C. elegans six, and Pristionchus pacificus only three cells that are competent to form Vulval tissue. In P. pacificus, programmed cell death of individual Vulval precursor cells alters the size of the Vulva equivalence group. Results We have identified the genes controlling this cell-death event and the molecular mechanism of the reduction of the Vulva equivalence group. Mutations in Ppa-hairy , a gene that is unknown from C. elegans , result in the survival of two precursor cells, which expands the Vulva equivalence group. Mutations in Ppa-groucho cause a similar phenotype. Ppa -HAIRY and Ppa -GROUCHO form a molecular module that represses the Hox gene Ppa-lin-39 and thereby reduces the size of the Vulva equivalence group. The C. elegans genome does not encode a similar hairy -like gene, and no typical HAIRY/GROUCHO module exists. Conclusions We conclude that the Vulva equivalence group in Pristionchus is patterned by a HAIRY/GROUCHO module, which is absent in Caenorhabditis . Thus, changes in the number, structure, and function of nematode hairy -like transcription factors are involved in the evolutionary alteration of this equivalence group.
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the pristionchus hox gene ppa lin 39 inhibits programmed cell death to specify the Vulva equivalence group and is not required during Vulval induction
Development, 1998Co-Authors: Ralf J Sommer, Andreas Eizinger, Benno Jungblut, A Bubeck, Isabel SchlakAbstract:In the two nematode species Caenorhabditis elegans and Pristionchus pacificus the Vulva equivalence group in the central body region is specified by the Hox gene lin-39. C. elegans lin-39 mutants are Vulvaless and the Vulval precursor cells fuse with the surrounding hypodermis, whereas in P. pacificus lin-39 mutants the Vulval precursor cells die by apoptosis. Mechanistically, LIN-39 might inhibit non-Vulval fate (cell fusion in C. elegans, apoptosis in P. pacificus), promote Vulval fate or do both. To study the mechanism of lin-39 function, we isolated P. pacificus cell death mutants and identified mutations in ced-3. Surprisingly, P. pacificus ced-3; lin-39 double mutants form a functional Vulva in the absence of LIN-39 activity. Thus, in P. pacificus lin-39 specifies the Vulva equivalence group by inhibiting programmed cell death. Furthermore, these data reveal an important difference in a later function of lin-39 between the two species. In C. elegans, LIN-39 specifies Vulval cell fates in response to inductive RAS signaling, and in P. pacificus LIN-39 is not required for Vulval induction. Thus, the comparative analysis indicates that lin-39 has distinct functions in both species although the gene is acting in a homologous developmental system.
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apoptosis and change of competence limit the size of the Vulva equivalence group in pristionchus pacificus a genetic analysis
Current Biology, 1996Co-Authors: Ralf J Sommer, Paul W. SternbergAbstract:Abstract Background: To understand how alterations in the molecular mechanisms underlying developmental processes generate a diversity of biological forms, comparative developmental biology can be combined with genetic analysis. The formation of the nematode Vulva is one tractable system for such evolutionary developmental analysis, as much is understood about its development in Caenorhabditis elegans . In Caenorhabditis , six of twelve ventral epidermal cells form the ‘Vulva equivalence group'; although all six cells are competent to adopt Vulval cell fates in response to an inductive signal, only three of these cells are induced to form Vulval tissue. Results In some species of the nematode families Rhabditidae, Neodiplogastridae and Panagrolaimidae, the number of cells in the Vulva equivalence group is limited by apoptosis and decreased responsiveness to inductive signals (competence). We have initiated a genetic analysis in one of these species, Pristionchus pacificus , to understand the evolution of the specification of ventral epidermal cells that are competent to generate the Vulva. A ped-4 mutation restores competence to an incompetent cell. Mutation of either of two other genes of Pristionchus cause two anterior cells that die in wild-type to survive. A ped-5 mutation causes these cells to be competent to respond to inductive signals, expanding the equivalence group. A ped-6 mutation causes these cells to form ectopic, anterior Vulva-like invaginations. Conclusion During nematode evolution, apoptosis and change of competence alter the number and potency of ventral epidermal cells. The phenotypes of Pristionchus mutants suggest that alterations in homeotic gene control of anteroposterior patterning is involved in creating this cellular diversity.
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evolution of cell lineage and pattern formation in the Vulval equivalence group of rhabditid nematodes
Developmental Biology, 1995Co-Authors: Ralf J Sommer, Paul W. SternbergAbstract:Abstract During the formation of the Vulva in many nematode hermaphrodites or females, pattern formation, induction, and cell specification can readily be studied at a single-cell level. Nematodes thus allow an evolutionary analysis of developmental processes. We have analyzed cell lineages and pattern formation in the Vulva equivalence group of six rhabditid nematodes of the genera Oscheius, Rhabditella, Rhabditoides, Pelodera, and Protorhabditis . The comparison of these species with four previously analyzed species of this family reveals evolutionary modification at several levels. The number of Vulva precursor cells (VPCs) differ among species. Of the three particular cell lineages (1°, 2°, and 3°) generated by the Vulva precursor cells in Caenorhabditis, two (2° and 3°) are altered, whereas the third lineage (1°) is conserved among the analyzed species. While most Vulval lineages are invariant, we observe variability of the 3° lineage in Pelodera with respect to the number of precursor cells adopting this fate and the number of progeny formed. In two species, the 3° lineage generates an asymmetrical set of cells, oriented by the gonad. In Protorhabditis we frequently find animals with an additional or altered set of VPCs forming Vulval tissue.
Paul W. Sternberg - One of the best experts on this subject based on the ideXlab platform.
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cis regulatory control of three cell fate specific genes in Vulval organogenesis of caenorhabditis elegans and c briggsae
Developmental Biology, 2003Co-Authors: Martha Kirouac, Paul W. SternbergAbstract:The great-grandprogeny of the Caenorhabditis elegans Vulval precursor cells (VPCs) adopt one of the final vulA, B1, B2, C, D, E, and F cell fates in a precise spatial pattern. This pattern of Vulval cell types is likely to depend on the cis-regulatory regions of the transcriptional targets of intercellular signals in Vulval development. egl-17, zmp-1, and cdh-3 are expressed differentially in the developing Vulva cells, providing a potential readout for different signaling pathways. To understand how such pathways interact to specify unique Vulval cell types in a precise pattern, we have identified cis-regulatory regions sufficient to confer Vulval cell type-specific regulation when fused in cis to the basal pes-10 promoter. We have identified the C. briggsae homologs of these three genes, with their corresponding control regions, and tested these regions in both C. elegans and C. briggsae. These regions of similarity in C. elegans and C. briggsae upstream of egl-17, zmp-1, and cdh-3 promote expression in Vulval cells and the anchor cell (AC). By using the cis-regulatory analysis and phylogenetic footprinting, we have identified overrepresented sequences involved in conferring Vulval and AC expression.
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apoptosis and change of competence limit the size of the Vulva equivalence group in pristionchus pacificus a genetic analysis
Current Biology, 1996Co-Authors: Ralf J Sommer, Paul W. SternbergAbstract:Abstract Background: To understand how alterations in the molecular mechanisms underlying developmental processes generate a diversity of biological forms, comparative developmental biology can be combined with genetic analysis. The formation of the nematode Vulva is one tractable system for such evolutionary developmental analysis, as much is understood about its development in Caenorhabditis elegans . In Caenorhabditis , six of twelve ventral epidermal cells form the ‘Vulva equivalence group'; although all six cells are competent to adopt Vulval cell fates in response to an inductive signal, only three of these cells are induced to form Vulval tissue. Results In some species of the nematode families Rhabditidae, Neodiplogastridae and Panagrolaimidae, the number of cells in the Vulva equivalence group is limited by apoptosis and decreased responsiveness to inductive signals (competence). We have initiated a genetic analysis in one of these species, Pristionchus pacificus , to understand the evolution of the specification of ventral epidermal cells that are competent to generate the Vulva. A ped-4 mutation restores competence to an incompetent cell. Mutation of either of two other genes of Pristionchus cause two anterior cells that die in wild-type to survive. A ped-5 mutation causes these cells to be competent to respond to inductive signals, expanding the equivalence group. A ped-6 mutation causes these cells to form ectopic, anterior Vulva-like invaginations. Conclusion During nematode evolution, apoptosis and change of competence alter the number and potency of ventral epidermal cells. The phenotypes of Pristionchus mutants suggest that alterations in homeotic gene control of anteroposterior patterning is involved in creating this cellular diversity.
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evolution of cell lineage and pattern formation in the Vulval equivalence group of rhabditid nematodes
Developmental Biology, 1995Co-Authors: Ralf J Sommer, Paul W. SternbergAbstract:Abstract During the formation of the Vulva in many nematode hermaphrodites or females, pattern formation, induction, and cell specification can readily be studied at a single-cell level. Nematodes thus allow an evolutionary analysis of developmental processes. We have analyzed cell lineages and pattern formation in the Vulva equivalence group of six rhabditid nematodes of the genera Oscheius, Rhabditella, Rhabditoides, Pelodera, and Protorhabditis . The comparison of these species with four previously analyzed species of this family reveals evolutionary modification at several levels. The number of Vulva precursor cells (VPCs) differ among species. Of the three particular cell lineages (1°, 2°, and 3°) generated by the Vulva precursor cells in Caenorhabditis, two (2° and 3°) are altered, whereas the third lineage (1°) is conserved among the analyzed species. While most Vulval lineages are invariant, we observe variability of the 3° lineage in Pelodera with respect to the number of precursor cells adopting this fate and the number of progeny formed. In two species, the 3° lineage generates an asymmetrical set of cells, oriented by the gonad. In Protorhabditis we frequently find animals with an additional or altered set of VPCs forming Vulval tissue.
Benjamin Schlager - One of the best experts on this subject based on the ideXlab platform.
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hairy like transcription factors and the evolution of the nematode Vulva equivalence group
Current Biology, 2006Co-Authors: Benjamin Schlager, Waltraud Roseler, Arturo Gutierrez, Min Zheng, Ralf J SommerAbstract:Summary Background Nematode Vulva formation provides a paradigm to study the evolution of pattern formation and cell-fate specification. The Caenorhabditis elegans Vulva is generated from three of six equipotent cells that form the so-called Vulva equivalence group. During evolution, the size of the Vulva equivalence group has changed: Panagrellus redivivus has eight, C. elegans six, and Pristionchus pacificus only three cells that are competent to form Vulval tissue. In P. pacificus, programmed cell death of individual Vulval precursor cells alters the size of the Vulva equivalence group. Results We have identified the genes controlling this cell-death event and the molecular mechanism of the reduction of the Vulva equivalence group. Mutations in Ppa-hairy , a gene that is unknown from C. elegans , result in the survival of two precursor cells, which expands the Vulva equivalence group. Mutations in Ppa-groucho cause a similar phenotype. Ppa -HAIRY and Ppa -GROUCHO form a molecular module that represses the Hox gene Ppa-lin-39 and thereby reduces the size of the Vulva equivalence group. The C. elegans genome does not encode a similar hairy -like gene, and no typical HAIRY/GROUCHO module exists. Conclusions We conclude that the Vulva equivalence group in Pristionchus is patterned by a HAIRY/GROUCHO module, which is absent in Caenorhabditis . Thus, changes in the number, structure, and function of nematode hairy -like transcription factors are involved in the evolutionary alteration of this equivalence group.
Masaki Mandai - One of the best experts on this subject based on the ideXlab platform.
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invasive paget s disease of the Vulva treated with a combination of surgery and concurrent chemoradiotherapy a case report
Current Opinion in Clinical Nutrition and Metabolic Care, 2018Co-Authors: Yoshihide Inayama, Kaoru Abiko, Taito Miyamoto, Akihito Horie, Ken Yamaguchi, Tsukasa Baba, Noriomi Matsumura, Sachiko Minamiguchi, Masaki MandaiAbstract:: Invasive Paget's disease of the Vulva (IP) is rare among patients with Vulvar cancer. Radiation therapy and chemotherapy are not considered as radical, whereas surgical resection of the tumor with abdominal lymphadenectomy is highly invasive. Thus, more effective and less invasive treatments for IP are required. The present study reports a case of a 64-year-old woman with IP, who was treated with a combination of surgery and concurrent chemoradiotherapy (CCRT). The patient was diagnosed with IP with suspected lymph node metastases to the inguinal and pelvic lymph nodes, after having suffered from pruritus Vulvae for 7 years. Following mapping biopsy, wide local excision, bilateral inguinal lymph node resection and laparoscopic pelvic lymphadenectomy were successfully performed. The Vulva was reconstructed with a local fat flap. Postoperative pathological examination revealed metastases to the bilateral superficial inguinal and the left obturator and lateral suprainguinal lymph nodes. Adjuvant CCRT (whole pelvic irradiation, 50.4 Gy with weekly cisplatin, 40 mg/m2) was completed without notable complications. Therefore, laparoscopic pelvic lymphadenectomy may be useful in determining the irradiation field for adjuvant CCRT in patients with advanced IP.
Waltraud Roseler - One of the best experts on this subject based on the ideXlab platform.
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hairy like transcription factors and the evolution of the nematode Vulva equivalence group
Current Biology, 2006Co-Authors: Benjamin Schlager, Waltraud Roseler, Arturo Gutierrez, Min Zheng, Ralf J SommerAbstract:Summary Background Nematode Vulva formation provides a paradigm to study the evolution of pattern formation and cell-fate specification. The Caenorhabditis elegans Vulva is generated from three of six equipotent cells that form the so-called Vulva equivalence group. During evolution, the size of the Vulva equivalence group has changed: Panagrellus redivivus has eight, C. elegans six, and Pristionchus pacificus only three cells that are competent to form Vulval tissue. In P. pacificus, programmed cell death of individual Vulval precursor cells alters the size of the Vulva equivalence group. Results We have identified the genes controlling this cell-death event and the molecular mechanism of the reduction of the Vulva equivalence group. Mutations in Ppa-hairy , a gene that is unknown from C. elegans , result in the survival of two precursor cells, which expands the Vulva equivalence group. Mutations in Ppa-groucho cause a similar phenotype. Ppa -HAIRY and Ppa -GROUCHO form a molecular module that represses the Hox gene Ppa-lin-39 and thereby reduces the size of the Vulva equivalence group. The C. elegans genome does not encode a similar hairy -like gene, and no typical HAIRY/GROUCHO module exists. Conclusions We conclude that the Vulva equivalence group in Pristionchus is patterned by a HAIRY/GROUCHO module, which is absent in Caenorhabditis . Thus, changes in the number, structure, and function of nematode hairy -like transcription factors are involved in the evolutionary alteration of this equivalence group.
