Genetic control of trichome branch number in Arabidopsis: the roles of the FURCA loci

Development ◽  
1999 ◽  
Vol 126 (24) ◽  
pp. 5547-5557 ◽  
Author(s):  
D. Luo ◽  
D.G. Oppenheimer
Keyword(s):  
Cell Shape ◽  
Genetic Interactions ◽  
Secondary Branch ◽  
Branch Number ◽  
Recessive Mutations ◽  
New Genes ◽  
Positive Regulators ◽  
Complementation Groups ◽  
Hair Morphogenesis ◽  
New Mutations

We are using trichome (hair) morphogenesis as a model to study how plant cell shape is controlled. During a screen for new mutations that affect trichome branch initiation in Arabidopsis, we identified seven new mutants that show a reduction in trichome branch number from three branches to two. These mutations were named furca, after the Latin word for two-pronged fork. These seven recessive mutations were placed into four complementation groups that define four new genes: FURCA1, FURCA2, FURCA3 and FURCA4. The trichome branch number phenotype indicates that the FURCA genes encode positive regulators of trichome branch initiation. Analysis of double mutants suggests that primary and secondary branch initiation events are not genetically distinct, but rely on the levels of partially redundant groups of regulators of trichome branch initiation. Based on the analysis of both epistatic and additive genetic interactions between the FURCA genes and other genes that control trichome branch number, we propose a model that explains how these genes interact to control trichome branch initiation. This model successfully predicts the phenotypes of all the single and double mutants examined and suggests points of control of the trichome branch pathway.

Mutations Causing Constitutive Invertase Synthesis in Yeast: Genetic Interactions with snf Mutations

Genetics ◽  
1987 ◽  
Vol 115 (2) ◽  
pp. 247-253
Author(s):  
Lenore Neigeborn ◽  
Marian Carlson
Keyword(s):  
Regulatory Region ◽  
Constitutive Expression ◽  
Genetic Interactions ◽  
The Third ◽  
Recessive Mutations ◽  
Constitutive Mutation ◽  
Complementation Groups ◽  
High Level ◽  
Yeast Genetic ◽  
Very High

ABSTRACT We have selected 210 mutants able to grow on sucrose in the presence of 2-deoxyglucose. We identified recessive mutations in three major complementation groups that cause constitutive (glucose-insensitive) secreted invertase synthesis. Two groups comprise alleles of the previously identified HXK2 and REG1 genes, and the third group was designated cid1 (constitutive invertase derepression). The effect of cid1 on SUC2 expression is mediated by the SUC2 upstream regulatory region, as judged by the constitutive expression of a SUC2-LEU2-lacZ fusion in which the LEU2 promoter is under control of SUC2 upstream sequences. A cid1 mutation also causes glucose-insensitive expression of maltase. The previously isolated constitutive mutation ssn6 is epistatic to cid1, reg1 and hxk2 for very high level constitutive invertase expression. Mutations in SNF genes that prevent derepression of invertase are epistatic to cid1, reg1 and hxk2; we have previously shown that ssn6 has different epistasis relationships with snf mutations. The constitutive mutation tup1 was found to resemble ssn6 in its genetic interactions with snf mutations. These findings suggest that CID1, REG1 and HXK2 are functionally distinct from SSN6 and TUP1.

scholarly journals Autosomal Mutations Affecting Adhesion Between Wing Surfaces in Drosophila melanogaster

Genetics ◽  
1997 ◽  
Vol 146 (1) ◽  
pp. 275-285 ◽  
Author(s):  
Mary Prout ◽  
Zubin Damania ◽  
Julie Soong ◽  
Dianne Fristrom ◽  
James W Fristrom
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Adhesion ◽  
Muscle Function ◽  
Genetic Interactions ◽  
New Genes ◽  
Evolutionarily Conserved ◽  
Dependent Cell ◽  
Integrin Gene ◽  
Complementation Groups ◽  
Cell To Cell Adhesion

Integrins are evolutionarily conserved transmembrane α,β heterodimeric receptors involved in cell-to-matrix and cell-to-cell adhesions. In Drosophila the position-specific (PS) integrins mediate the formation and maintenance of junctions between muscle and epidermis and between the two epidermal wing surfaces. Besides integrins, other proteins are implicated in integrin-dependent adhesion. In Drosophila, somatic clones of mutations in PS integrin genes disrupt adhesion between wing surfaces to produce wing blisters. To identify other genes whose products function in adhesion between wing surfaces, we conducted a screen for autosomal mutations that produce blisters in somatic wing clones. We isolated 76 independent mutations in 25 complementation groups, 15 of which contain more than one allele. Chromosomal sites were determined by deficiency mapping, and genetic interactions with mutations in the βPS integrin gene myospheroid were investigated. Mutations in four known genes (blistered, Delta, dumpy and mastermind) were isolated. Mutations were isolated in three new genes (piopio, rhea and steamer duck) that affect myo-epidermal junctions or muscle function in embryos. Mutations in three other genes (kakapo, kiwi and moa) may also affect cell adhesion or muscle function at hatching. These new mutants provide valuable material for the study of integrin-dependent cell-to-cell adhesion.

scholarly journals Multiple new genes that determine activity for the first step of leucine biosynthesis in Saccharomyces cerevisiae.

Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 13-20 ◽  
Author(s):  
P Drain ◽  
P Schimmel
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Wild Type ◽  
Leucine Biosynthesis ◽  
Yeast Saccharomyces Cerevisiae ◽  
Multiple Components ◽  
New Genes ◽  
Yeast Strains ◽  
Complementation Groups ◽  
Or Genes ◽  
New Mutations

Abstract The first step in the biosynthesis of leucine is catalyzed by alpha-isopropylmalate (alpha-IPM) synthase. In the yeast Saccharomyces cerevisiae, LEU4 encodes the isozyme responsible for the majority of alpha-IPM synthase activity. Yeast strains that bear disruption alleles of LEU4, however, are Leu+ and exhibit a level of synthase activity that is 20% of the wild type. To identify the gene or genes that encode this remaining activity, a leu4 disruption strain was mutagenized. The mutations identified define three new complementation groups, designated leu6, leu7 and leu8. Each of these new mutations effect leucine auxotrophy only if a leu4 mutation is present and each results in loss of alpha-IPM synthase activity. Further analysis suggests that LEU7 and LEU8 are candidates for the gene or genes that encode an alpha-IPM synthase activity. The results demonstrate that multiple components determine the residual alpha-IPM synthase activity in leu4 gene disruption strains of S. cerevisiae.

scholarly journals Mutations in rik1, clr2, clr3 and clr4 genes asymmetrically derepress the silent mating-type loci in fission yeast.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 53-64
Author(s):  
K Ekwall ◽  
T Ruusala
Keyword(s):  
Mating Type ◽  
Dna Sequences ◽  
Recessive Mutations ◽  
New Genes ◽  
Genes Encoding ◽  
Active Locus ◽  
Mating Type Genes ◽  
Type Information ◽  
New Mutations ◽  
Silent Mating Type Loci

Abstract In Schizosaccharomyces pombe the mating-type information is stored at two transcriptionally silent loci (mat2 and mat3). The region between these sites (K region) is inert for meiotic crossing over. The mating-type genes (M or P) are expressed only when present at a third, active locus (mat1). We have earlier shown that the positional regulation of P genes is based on repression at the silent site, caused by elements in the flanking DNA sequences. In this study we have mutagenized a sterile mat1 deleted strain and selected for cells that are able to conjugate. Recessive mutations of this type should define genes encoding trans-acting factors involved in repression of the silent mating-type loci. Before this work mutations in two genes, clr1 and swi6, had been shown to allow both expression of the silent loci and recombination in the K region. The sensitivity of the present selection is demonstrated by the isolation of new mutations that derepress one or both of the silent loci (M-mating or bi-mating). The frequency of M-mating mutants was almost two orders of magnitude higher than that of bi-mating mutants and in all mutants analyzed mat3-M expression was significantly higher than mat2-P expression. The mutations define three new genes, clr2, clr3 and clr4. In addition we show that the rik1 mutant previously known to allow recombination in the K region also depresses the silent loci.

scholarly journals New SNF genes, GAL11 and GRR1 affect SUC2 expression in Saccharomyces cerevisiae.

Genetics ◽  
1991 ◽  
Vol 129 (3) ◽  
pp. 675-684 ◽  
Author(s):  
L G Vallier ◽  
M Carlson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Null Mutation ◽  
Wild Type ◽  
Glucose Limitation ◽  
Wild Type Level ◽  
Recessive Mutations ◽  
New Genes ◽  
Complementation Groups ◽  
Invertase Gene ◽  
Inducible Gene

Abstract To identify new genes required for depression of the SUC2 (invertase) gene in Saccharomyces cerevisiae, we have isolated mutants with defects in raffinose utilization. In addition to mutations in SUC2 and previously identified SNF genes, we recovered recessive mutations that define four new complementation groups, designated snf7 through snf10. These mutations cause defects in the derepression of SUC2 in response to glucose limitation. We also recovered five alleles of gal11 and showed that a gal11 null mutation decreases SUC2 expression to 30% of the wild-type level. Finally, one of the mutants carries a grr1 allele that converts SUC2 from a glucose-inducible gene.

Interacting genes required for pharyngeal excitation by motor neuron MC in Caenorhabditis elegans.

Genetics ◽  
1995 ◽  
Vol 141 (4) ◽  
pp. 1365-1382 ◽  
Author(s):  
D M Raizen ◽  
R Y Lee ◽  
L Avery
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Interactions ◽  
Neuron Type ◽  
Loss Of Function ◽  
Ach Release ◽  
Pharyngeal Muscle ◽  
Recessive Mutations ◽  
Allele Specific ◽  
Pharyngeal Pumping ◽  
Pumping Rates

Abstract We studied the control of pharyngeal excitation in Caenorhabditis elegans. By laser ablating subsets of the pharyngeal nervous system, we found that the MC neuron type is necessary and probably sufficient for rapid pharyngeal pumping. Electropharyngeograms showed that MC transmits excitatory postsynaptic potentials, suggesting that MC acts as a neurogenic pacemaker for pharyngeal pumping. Mutations in genes required for acetylcholine (ACh) release and an antagonist of the nicotinic ACh receptor (nAChR) reduced pumping rates, suggesting that a nAChR is required for MC transmission. To identify genes required for MC neurotransmission, we screened for mutations that cause slow pumping but no other defects. Mutations in two genes, eat-2 and eat-18, eliminated MC neurotransmission. A gain-of-function eat-18 mutation, ad820sd, and a putative loss-of-function eat-18 mutation, ad1110, both reduced the excitation of pharyngeal muscle in response to the nAChR agonists nicotine and carbachol, suggesting that eat-18 is required for the function of a pharyngeal nAChR. Fourteen recessive mutations in eat-2 fell into five complementation classes. We found allele-specific genetic interactions between eat-2 and eat-18 that correlated with complementation classes of eat-2. We propose that eat-18 and eat-2 function in a multisubunit protein complex involved in the function of a pharyngeal nAChR.

scholarly journals Extragenic suppressors of the arabidopsis zwi-3 mutation identify new genes that function in trichome branch formation and pollen tube growth

Development ◽  
1999 ◽  
Vol 126 (14) ◽  
pp. 3079-3088 ◽  
Author(s):  
S. Krishnakumar ◽  
D.G. Oppenheimer
Keyword(s):  
Pollen Tube ◽  
Pollen Tube Growth ◽  
Mutational Analysis ◽  
Negative Regulator ◽  
Tube Growth ◽  
Tail Domain ◽  
Branch Number ◽  
New Genes ◽  
Allele Specific ◽  
Extragenic Suppressors

The plant cytoskeleton plays a pivotal role in determining the direction of cell wall expansion, and ultimately the cell's final shape. However, the mechanisms by which localized expansion events are initiated remain obscure. Mutational analysis of the trichome (plant hair) morphogenic pathway in Arabidopsis has identified at least eight genes that determine trichome branch number. One of these genes, ZWICHEL (ZWI), encodes a novel member of the kinesin superfamily of motor proteins. Mutations in the ZWI gene cause a reduction in the number of trichome branches. To identify additional genes involved in trichome branch initiation, we screened for extragenic suppressors of the zwi-3 mutation and isolated three suppressors that rescued the branch number defect of zwi-3. These suppressors define three genes, named suz, for suppressor of zwichel-3. All of the suppressors were shown to be allele specific. One of the suppressors, suz2, also rescued the trichome branch number defect of another branch mutant, furca1-2. Plants homozygous for suz2 have more than the wild-type number of trichome branches. This suggests that SUZ2 is a negative regulator of trichome branching and may interact with ZWI and FURCA1. The suz1 and suz3 mutants display no obvious phenotype in the absence of the zwi-3 mutation. The suz1 zwi-3 double mutants also exhibited a male-sterile phenotype due to a defect in pollen tube germination and growth, whereas both the suz1 and the zwi-3 single mutants are fertile. The synthetic male sterility of the suz1 zwi-3 double mutants suggests a role for SUZ1 and ZWI in pollen germination and pollen tube growth. DNA sequence analysis of the zwi-3 mutation indicated that only the tail domain of the zwi-3 protein would be expressed. Thus, the suz mutations show allele-specific suppression of a kinesin mutant that lacks the motor domain.

Cell morphogenesis of trichomes in Arabidopsis: differential control of primary and secondary branching by branch initiation regulators and cell growth

Development ◽  
1997 ◽  
Vol 124 (19) ◽  
pp. 3779-3786 ◽  
Author(s):  
U. Folkers ◽  
J. Berger ◽  
M. Hulskamp
Keyword(s):  
Cell Growth ◽  
Cell Shape ◽  
Normal Development ◽  
Branching Pattern ◽  
Cell Morphogenesis ◽  
Negative Regulators ◽  
Branch Number ◽  
Underlying Mechanisms ◽  
Differential Control ◽  
Trichome Cell

Cell morphogenesis, i.e. the acquisition of a particular cell shape, can be examined genetically in the three-branched trichomes that differentiate from single epidermal cells on the leaves of Arabidopsis thaliana. In normal development, the growing trichome cell undergoes two successive branching events, resulting in a proximal side stem and a distal main stem which subsequently splits in two branches. Using new and previously described trichome mutants, we have analyzed the branching pattern in single and double mutants affecting branch number or cell size in order to determine underlying mechanisms. Our results suggest that primary branching is genetically distinct from subsequent branching events and that the latter, secondary events are initiated in response to positive and negative regulators of branching as well as subject to control by cell growth. We propose a model of how trichome cell morphogenesis is regulated during normal development.

scholarly journals Identification and Characterization of Genes Required for Early Myxococcus xanthus Developmental Gene Expression

2000 ◽  
Vol 182 (16) ◽  
pp. 4564-4571 ◽  
Author(s):  
Dongchuan Guo ◽  
Yun Wu ◽  
Heidi B. Kaplan
Keyword(s):  
Response Regulator ◽  
Myxococcus Xanthus ◽  
Normal Growth ◽  
Negative Regulator ◽  
Developmental Expression ◽  
Wild Type ◽  
Developmental Gene ◽  
O Antigen ◽  
New Genes ◽  
Positive Regulators

ABSTRACT Starvation and cell density regulate the developmental expression of Myxococcus xanthus gene 4521. Three classes of mutants allow expression of this developmental gene during growth on nutrient agar, such that colonies of strains containing a Tn5 lac Ω4521 fusion are Lac+. One class of these mutants inactivates SasN, a negative regulator of 4521expression; another class activates SasS, a sensor kinase-positive regulator of 4521 expression; and a third class blocks lipopolysaccharide (LPS) O-antigen biosynthesis. To identify additional positive regulators of 4521 expression, 11 Lac− TnV.AS transposon insertion mutants were isolated from a screen of 18,000 Lac+ LPS O-antigen mutants containing Tn5 lac Ω4521 (Tcr). Ten mutations identified genes that could encode positive regulators of4521 developmental expression based on their ability to abolish 4521 expression during development in the absence of LPS O antigen and in an otherwise wild-type background. Eight of these mutations mapped to the sasB locus, which encodes the known 4521 regulators SasS and SasN. One mapped tosasS, whereas seven identified new genes. Three mutations mapped to a gene encoding an NtrC-like response regulator homologue, designated sasR, and four others mapped to a gene designated sasP. One mutation, designatedssp10, specifically suppressed the LPS O-antigen defect; the ssp10 mutation had no effect on 4521expression in an otherwise wild-type background but reduced4521 developmental expression in the absence of LPS O antigen to a level close to that of the parent strain. All of the mutations except those in sasP conferred defects during growth and development. These data indicate that a number of elements are required for 4521 developmental expression and that most of these are necessary for normal growth and fruiting body development.

scholarly journals Yeast mutants sensitive to antimicrotubule drugs define three genes that affect microtubule function.

Genetics ◽  
1990 ◽  
Vol 124 (2) ◽  
pp. 251-262 ◽  
Author(s):  
T Stearns ◽  
M A Hoyt ◽  
D Botstein
Keyword(s):  
Chromosome Loss ◽  
Gene Products ◽  
Wild Type ◽  
Tubulin Genes ◽  
New Genes ◽  
Complementation Groups ◽  
Yeast Mutants ◽  
Antimicrotubule Drugs ◽  
Tubulin Mutations ◽  
Microtubule Function

Abstract Three new genes affecting microtubule function in Saccharomyces cerevisiae were isolated by screening for mutants displaying supersensitivity to the antimicrotubule drug benomyl. Such mutants fall into six complementation groups: TUB1, TUB2 and TUB3, the three tubulin genes of yeast, and three new genes, which we have named CIN1, CIN2 and CIN4. Mutations in each of the CIN genes were also independently isolated by screening for mutants with increased rates of chromosome loss. Strains bearing mutations in the CIN genes are approximately tenfold more sensitive than wild type to both benomyl and to the related antimicrotubule drug, nocodazole. This phenotype is recessive for all alleles isolated. The CIN1, CIN2 and CIN4 genes were cloned by complementation of the benomyl-supersensitive phenotype. Null mutants of each of the genes are viable, and have phenotypes similar to those of the point mutants. Genetic evidence for the involvement of the CIN gene products in microtubule function comes from the observation that some tubulin mutations are suppressed by cin mutations, while other tubulin mutations are lethal in combination with cin mutations. Additional genetic experiments with cin mutants suggest that the three genes act together in the same pathway or structure to affect microtubule function.

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