scholarly journals Deletion of ptn1, a PTEN/TEP1 Orthologue, in Ustilago maydis Reduces Pathogenicity and Teliospore Development

2018 ◽  
Vol 5 (1) ◽  
pp. 1 ◽  
Author(s):  
Lalu Vijayakrishnapillai ◽  
John Desmarais ◽  
Michael Groeschen ◽  
Michael Perlin
Keyword(s):  
Defense Mechanisms ◽  
Developmental Process ◽  
Signal Transduction Pathway ◽  
Ustilago Maydis ◽  
Suppressor Gene ◽  
Tumor Formation ◽  
Proliferation And Apoptosis ◽  
Mating Efficiency ◽  
Percent Germination

The PTEN/PI3K/mTOR signal transduction pathway is involved in the regulation of biological processes such as metabolism, cell growth, cell proliferation, and apoptosis. This pathway has been extensively studied in mammals, leading to the conclusion that PTEN is a major tumor suppressor gene. PTEN orthologues have been characterized in a variety of organisms, both vertebrates and non-vertebrates, and studies of the associated PTEN/PI3K/mTOR pathway indicate that it is widely conserved. Studies in fungal systems indicated a role of PTEN in fungal defense mechanisms in Candida albicans, and in the developmental process of sporulation in Saccharomyces cerevisiae. The present study was aimed at investigating the role of the PTEN ortholog, ptn1, in Ustilago maydis, the pathogen of maize. U. maydis ptn1 mutant strains where ptn1 gene is deleted or overexpressed were examined for phenotypes associate with mating, virulence and spore formation. While the overexpression of ptn1 had no substantial effects on virulence, ptn1 deletion strains showed slight reductions in mating efficiency and significant reductions in virulence; tumor formation on stem and/or leaves were severely reduced. Moreover, tumors, when present, had significantly lower levels of mature teliospores, and the percent germination of such spores was similarly reduced. Thus, ptn1 is required for these important aspects of virulence in this fungus.

The role of the Wilms' tumour-suppressor protein WT1 in apoptosis

2008 ◽  
Vol 36 (4) ◽  
pp. 629-631 ◽  
Author(s):  
Jörg Hartkamp ◽  
Stefan G.E. Roberts
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Suppressor Gene ◽  
Tumour Suppressor Gene ◽  
Tumour Suppressor ◽  
Wilms Tumour ◽  
Zinc Finger Transcription Factor ◽  
Tumour Suppressor Protein ◽  
Proliferation And Apoptosis

The Wilms' tumour-suppressor gene (WT1), encodes a zinc-finger transcription factor that is critical for the development of several organs, including the kidneys, gonads and spleen. Despite its identification as a tumour suppressor that plays a crucial role in the formation of a paediatric malignancy of the kidneys (Wilms' tumour), it has also emerged as an oncogenic factor influencing proliferation and apoptosis in a large variety of adult cancers. This review focuses on new insights into WT1's role in early development and its potential oncogenic role in adult cancer.

Expression of p53 Protein in Pterygium

1998 ◽  
Vol 8 (3) ◽  
pp. 157-161 ◽  
Author(s):  
C. Onur ◽  
D. Orhan ◽  
M. Orhan ◽  
S. Dizbay Sak ◽  
Ö. Tulunay ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Uv Radiation ◽  
P53 Protein ◽  
Suppressor Gene ◽  
Tumor Formation ◽  
Nuclear Staining ◽  
P53 Tumor Suppressor ◽  
P53 Tumor Suppressor Gene

Purpose The pathogenesis of pterygium is still not completely understood and many environmental factors, including ultraviolet (UV) radiation, play an important role in its etiology. Chronic exposure to UV radiation causes mutations in the p53 tumor suppressor gene, eventually leading to tumor formation. We analyzed the immunohistochemical expression of p53 proteins in pterygial tissues to determine the role of the p53 tumor suppressor gene in the development of pterygium. Methods Pterygial specimens were studied immunohistochemically using antibodies against p53 protein. Results Out of 38 specimens studied, 35 (92.1%) had conjunctival epithelial cells without p53 specific nuclear staining. Only three specimens (7.9%) had a few p53 stained cells. The role of UV radiation in the pathogenesis of pterygium is supported by epidemiological, geographical and microscopic findings. However, our results are not consistent with these data on a genetic basis. Conclusions We conclude that defective p53 tumor suppressor gene function seems to have no role in the pathogenesis of pterygium.

scholarly journals The Mitochondrial Dnm1-Like Fission Component Is Required for lga2 -Induced Mitophagy but Dispensable for Starvation-Induced Mitophagy in Ustilago maydis

2012 ◽  
Vol 11 (9) ◽  
pp. 1154-1166 ◽  
Author(s):  
Fernanda Nieto-Jacobo ◽  
Denise Pasch ◽  
Christoph W. Basse
Keyword(s):  
Sexual Development ◽  
Fluorescent Protein ◽  
Developmental Process ◽  
Mitochondrial Fission ◽  
Mitochondrial Protein ◽  
Ustilago Maydis ◽  
Mitochondrial Rna ◽  
Type Locus ◽  
Content Type

ABSTRACT Selective elimination of mitochondria by autophagy (mitophagy) is a crucial developmental process to dispose of disintegrated or superflous organelles. However, little is known about underlying regulatory mechanisms. We have investigated mitophagy in response to conditional overexpression of the a2 mating-type locus gene lga2 , which encodes a small mitochondrial protein critically involved in uniparental mitochondrial DNA inheritance during sexual development of Ustilago maydis . In this study, we show that conditional overexpression of lga2 efficiently triggers mitophagy that is dependent on atg8 and atg11 , consistent with selective autophagy. lga2 -triggered mitophagy is preceded by mitochondrial dysfunction, including depletion of mitochondrial RNA transcripts, and is mechanistically distinct from starvation-induced mitophagy despite a common requirement for atg11 . In particular, lga2 -triggered mitophagy strongly depends on the mitochondrial fission factor Dnm1, but it is only slightly affected by N -acetylcysteine, which is an inhibitor of starvation-induced mitophagy. To further delineate the role of mitochondrial fission, we analyzed lga2 effects in Δfis1 mutants. This revealed that mitochondrial fragmentation was only attenuated and mitophagy was largely unaffected. In further support of a Fis1-independent role for Dnm1, mitochondrial association of green fluorescent protein-tagged Dnm1 as well as Dnm1-opposed mitochondrial fusion during sexual development were fis1 independent. In conclusion, our results specify the role of the mitochondrial fission factor Dnm1 in mitophagy and uncover differences between mitophagy pathways in the same cellular system.

scholarly journals Drosophila Immunity: Analysis of Larval Hemocytes by P-Element-Mediated Enhancer Trap

Genetics ◽  
1997 ◽  
Vol 147 (2) ◽  
pp. 623-634 ◽  
Author(s):  
Anne Braun ◽  
Bruno Lemaitre ◽  
René Lanot ◽  
Daniel Zachary ◽  
Marie Meister
Keyword(s):  
Defense Mechanisms ◽  
Tumor Formation ◽  
P Element ◽  
Lacz Expression ◽  
Hematopoietic Organ ◽  
Lymph Glands ◽  
New Genes ◽  
Tumor Phenotype ◽  
Third Line

Our aim was to identify new genes involved in the cellular aspects of defense mechanisms of Drosophila, as well as in melanotic tumor formation processes that are linked to blood cell disregulation. We have screened 1341 enhancer detector fly lines for expression of the lacZ reporter gene in larval hemocytes at the end of the third instar. We have selected 21 lines in which we observed a reproducible lacZ expression in blood cells. These lines were classified according to the subsets of hemocytes in which lacZ was expressed, and we identified five lines that can be used as lamellocyte markers. Three lines were selected for further analysis. The first exhibited strong lacZ expression in all lamellocytes. The second expressed lacZ in plasmatocytes and lamellocytes, and exhibited a melanotic tumor phenotype in larvae homozygous for the insertion. A third line showed a striking insertion-linked phenotype of melanized lymph glands (the hematopoietic organ), which resulted in the total absence of circulating hemocytes in the mutant larvae. We anticipate that this mutation, which we named domino, will prove a useful tool in the analysis of the role of hemocytes during the various aspects of immune response and melanotic tumor formation.

scholarly journals Role of Metastasis Suppressor KAI1/CD82 in Different Cancers

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Wei Yan ◽  
Jinny Huang ◽  
Qian Zhang ◽  
Jian Zhang
Keyword(s):  
Poor Prognosis ◽  
Tumor Metastasis ◽  
Malignant Tumors ◽  
Suppressor Gene ◽  
Tumor Formation ◽  
Metastasis Suppressor ◽  
Metastasis Suppressor Gene ◽  
Metastasis Suppressor Genes ◽  
Potential Strategy

Metastasis is one of the characteristics of malignant tumors and the main cause of death worldwide. The process of metastasis is mainly affected by tumor metastasis genes, tumor metastasis suppressor genes, tumor microenvironment, extracellular matrix degradation, and other factors. Thus, it is essential to elucidate the mechanism of metastasis and find the therapeutic targets in order to prevent the development of malignant tumors. KAI1/CD82, a member of tetraspanin superfamily of glycoproteins, has been reported as a tumor metastasis suppressor gene in various types of cancers without affecting the tumor formation. Many studies have demonstrated that low expression of KAI1/CD82 might lead to poor prognosis due to its interactions with other tetraspanins and integrins, resulting in the regulation of cell motility and invasion, cell-cell adhesion, and apoptosis. Considering its pathological and physiological significance, KAI1/CD82 could be a potential strategy for clinical predicting and preventing tumor progression and metastasis. The present review aims to discuss the role of KAI1/CD82 in metastasis for different cancers and examine its prospects as a metastasis biomarker and a therapeutic target.

Potential of Mesenchymal Stem Cells in Anti-Cancer Therapies

2020 ◽  
Vol 15 (6) ◽  
pp. 482-491 ◽  
Author(s):  
Milena Kostadinova ◽  
Milena Mourdjeva
Keyword(s):  
Cancer Cells ◽  
Small Population ◽  
Tumor Formation ◽  
Bioactive Molecules ◽  
Cancer Therapies ◽  
New Methods ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Blocking Mechanisms

Mesenchymal stem/stromal cells (MSCs) are localized throughout the adult body as a small population in the stroma of the tissue concerned. In injury, tissue damage, or tumor formation, they are activated and leave their niche to migrate to the site of injury, where they release a plethora of growth factors, cytokines, and other bioactive molecules. With the accumulation of data about the interaction between MSCs and tumor cells, the dualistic role of MSCs remains unclear. However, a large number of studies have demonstrated the natural anti-tumor properties inherent in MSCs, so this is the basis for intensive research for new methods using MSCs as a tool to suppress cancer cell development. This review focuses specifically on advanced approaches in modifying MSCs to become a powerful, precision- targeted tool for killing cancer cells, but not normal healthy cells. Suppression of tumor growth by MSCs can be accomplished by inducing apoptosis or cell cycle arrest, suppressing tumor angiogenesis, or blocking mechanisms mediating metastasis. In addition, the chemosensitivity of cancer cells may be increased so that the dose of the chemotherapeutic agent used could be significantly reduced.

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