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Mutant

About: Mutant is a research topic. Over the lifetime, 74520 publications have been published within this topic receiving 3477079 citations.


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Journal ArticleDOI
14 Jun 1996-Cell
TL;DR: The mutant phenotype suggests that G1-to-S phase progression is accelerated, overriding mechanisms for mitotic arrest and producing abnormally small cells in C. elegans.

465 citations

Journal ArticleDOI
01 Jan 1996-Planta
TL;DR: The morphology and anatomy of mp mutant plants throughout the Arabidopsis life cycle suggest that the MP gene promotes cell axialization and cell file formation at multiple stages of plant development.
Abstract: In the embryo of Arabidopsis thaliana (L.) Heynh., formation of the hypocotyl/root axis is initiated at the early-globular stage, recognizable as oriented expansion of formerly isodiametric cells. The process depends on the activity of the gene MONOPTEROS (MP); mp mutant embryos fail to produce hypocotyl and radicle. We have analyzed the morphology and anatomy of mp mutant plants throughout the Arabidopsis life cycle. Mutants form largely normal rosettes and root systems, but inflorescences either fail to form lateral flowers or these flowers are greatly reduced. Furthermore, the auxin transport capacity of inflorescence axes is impaired and the vascular strands in all analyzed organs are distorted. These features of the mutant phenotype suggest that the MP gene promotes cell axialization and cell file formation at multiple stages of plant development.

465 citations

Journal ArticleDOI
19 Oct 2001-Science
TL;DR: Findings show that C. elegansp53 mediates multiple stress responses in the soma, and mediates apoptosis and meiotic chromosome segregation in the germ line, and cep-1mutants show hypersensitivity to hypoxia-induced lethality and decreased longevity in response to starvation-induced stress.
Abstract: We have identified a homolog of the mammalian p53 tumor suppressor protein in the nematode Caenorhabditis elegans that is expressed ubiquitously in embryos. The gene encoding this protein, cep-1, promotes DNA damage-induced apoptosis and is required for normal meiotic chromosome segregation in the germ line. Moreover, although somatic apoptosis is unaffected, cep-1 mutants show hypersensitivity to hypoxia-induced lethality and decreased longevity in response to starvation-induced stress. Overexpression of CEP-1 promotes widespread caspase-independent cell death, demonstrating the critical importance of regulating p53 function at appropriate levels. These findings show that C. elegans p53 mediates multiple stress responses in the soma, and mediates apoptosis and meiotic chromosome segregation in the germ line.

464 citations

Journal ArticleDOI
TL;DR: Yeast two‐hybrid screening revealed that MKS1 interacts with the WRKY transcription factors WRKY25 and WRKY33, and may contribute to MPK4‐regulated defense activation by coupling the kinase to specific WR KY transcription factors.
Abstract: Arabidopsis MAP kinase 4 (MPK4) functions as a regulator of pathogen defense responses, because it is required for both repression of salicylic acid (SA)-dependent resistance and for activation of jasmonate (JA)-dependent defense gene expression. To understand MPK4 signaling mechanisms, we used yeast two-hybrid screening to identify the MPK4 substrate MKS1. Analyses of transgenic plants and genome-wide transcript profiling indicated that MKS1 is required for full SA-dependent resistance in mpk4 mutants, and that overexpression of MKS1 in wild-type plants is sufficient to activate SA-dependent resistance, but does not interfere with induction of a defense gene by JA. Further yeast two-hybrid screening revealed that MKS1 interacts with the WRKY transcription factors WRKY25 and WRKY33. WRKY25 and WRKY33 were shown to be in vitro substrates of MPK4, and a wrky33 knockout mutant was found to exhibit increased expression of the SA-related defense gene PR1. MKS1 may therefore contribute to MPK4-regulated defense activation by coupling the kinase to specific WRKY transcription factors.

463 citations

Journal ArticleDOI
TL;DR: Deregulation of these processes caused by mutations in APC is implicated in the initiation and expansion of colon cancer.
Abstract: The adenomatous polyposis coli (APC) gene is a key tumor suppressor gene. Mutations in the gene have been found not only in most colon cancers but also in some other cancers, such as those of the liver. The APC gene product is a 312 kDa protein that has multiple domains, through which it binds to various proteins, including beta-catenin, axin, CtBP, Asefs, IQGAP1, EB1 and microtubules. Studies using mutant mice and cultured cells have demonstrated that APC suppresses canonical Wnt signalling, which is essential for tumorigenesis, development and homeostasis of a variety of cell types, such as epithelial and lymphoid cells. Further studies have suggested that APC plays roles in several other fundamental cellular processes. These include cell adhesion and migration, organization of the actin and microtubule networks, spindle formation and chromosome segregation. Deregulation of these processes caused by mutations in APC is implicated in the initiation and expansion of colon cancer.

462 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20241
20237,150
20226,747
20211,630
20201,916
20191,849