Function and chromosomal location of the Cochliobolus heterostrophus TOX1 locus

1995 ◽  
Vol 73 (S1) ◽  
pp. 1071-1076 ◽  
Author(s):  
B. G. Turgeon ◽  
M. Kodama ◽  
G. Yang ◽  
M.S. Rose ◽  
S.W. Lu ◽  
...  
Keyword(s):  
Polyketide Synthase ◽  
Chromosomal Location ◽  
Genetic Locus ◽  
Single Gene ◽  
Molecular Genetic ◽  
Cochliobolus Heterostrophus ◽  
Male Sterile ◽  
Genetic Analyses ◽  
High Virulence ◽  
The Difference

Conventional genetic analyses have firmly established that the difference in virulence between race T and O of the corn pathogen Cochliobolus heterostrophus is determined by a single genetic locus called Tox1, which also controls production of T-toxin, a polyketide specifically toxic to corn with Texas male sterile (T) cytoplasm. More recently, molecular genetic analyses have revealed that Tox1 is not a single gene but rather at least two genetic loci situated on two different chromosomes. DNA at both of these loci is required for the biosynthesis of T-toxin and for the high virulence of race T to corn carrying T-cytoplasm. One of the loci encodes a polyketide synthase that is necessary for the assembly of the T-toxin molecule. Key words: polyketide, restriction enzyme mediated integration (REMI), host-specific toxin, corn, fungus, virulence.

scholarly journals Six New Genes Required for Production of T-Toxin, a Polyketide Determinant of High Virulence of Cochliobolus heterostrophus to Maize

2010 ◽  
Vol 23 (4) ◽  
pp. 458-472 ◽  
Author(s):  
Patrik Inderbitzin ◽  
Thipa Asvarak ◽  
B. Gillian Turgeon
Keyword(s):  
Evolutionary History ◽  
Phylogenetic Profile ◽  
Toxin Production ◽  
Gene Signature ◽  
Cochliobolus Heterostrophus ◽  
Male Sterile ◽  
Toxin A ◽  
New Genes ◽  
Unknown Protein ◽  
High Virulence

Southern Corn Leaf Blight, one of the worst plant disease epidemics in modern history, was caused by Cochliobolus heterostrophus race T, which produces T-toxin, a determinant of high virulence to maize carrying Texas male sterile cytoplasm. The genetics of T-toxin production is complex and the evolutionary origin of associated genes is uncertain. It is known that ability to produce T-toxin requires three genes encoded at two unlinked loci, Tox1A and Tox1B, which map to the breakpoints of a reciprocal translocation. DNA associated with Tox1A and Tox1B sums to about 1.2 Mb of A+T rich, repeated DNA that is not found in less virulent race O or other Cochliobolus species. Here, we describe identification and targeted deletion of six additional genes, three mapping to Tox1A and three to Tox1B. Mutant screens indicate that all six genes are involved in T-toxin production and high virulence to maize. The nine known Tox1 genes encode two polyketide synthases (PKS), one decarboxylase, five dehydrogenases, and one unknown protein. Only two have a similar phylogenetic profile. To trace evolutionary history of one of the core PKS, DNA from more than 100 Dothideomycete species were screened for homologs. An ortholog (60% identity) was confirmed in Didymella zeae-maydis, which produces PM-toxin, a polyketide of similar structure and biological specificity as T-toxin. Only one additional Dothideomycete species, the dung ascomycete Delitschia winteri harbored a paralog. The unresolved evolutionary history and distinctive gene signature of the PKS (fast-evolving, discontinuous taxonomic distribution) leaves open the question of lateral or vertical transmission.

scholarly journals Two Polyketide Synthase-Encoding Genes Are Required for Biosynthesis of the Polyketide Virulence Factor, T-toxin, by Cochliobolus heterostrophus

2006 ◽  
Vol 19 (2) ◽  
pp. 139-149 ◽  
Author(s):  
Scott E. Baker ◽  
Scott Kroken ◽  
Patrik Inderbitzin ◽  
Thipa Asvarak ◽  
Bi-Yu Li ◽  
...  
Keyword(s):  
Polyketide Synthase ◽  
Toxin Production ◽  
Carbon Chain ◽  
Cochliobolus Heterostrophus ◽  
Maize Production ◽  
High Virulence ◽  
Encoding Gene ◽  
Corn Leaf Blight ◽  
Encoding Genes ◽  
Sequencing Procedure

Cochliobolus heterostrophus race T, causal agent of southern corn leaf blight, requires T-toxin (a family of C35 to C49 polyketides) for high virulence on T-cytoplasm maize. Production of T-toxin is controlled by two unlinked loci, Tox1A and Tox1B, carried on 1.2 Mb of DNA not found in race O, a mildly virulent form of the fungus that does not produce T-toxin, or in any other Cochliobolus spp. or closely related fungus. PKS1, a polyketide synthase (PKS)-encoding gene at Tox1A, and DEC1, a decarboxylase-encoding gene at Tox1B, are necessary for T-toxin production. Although there is evidence that additional genes are required for Ttoxin production, efforts to clone them have been frustrated because the genes are located in highly repeated, A+T-rich DNA. To overcome this difficulty, ligation specificity-based expression analysis display (LEAD), a comparative amplified fragment length polymorphism/gel fractionation/capillary sequencing procedure, was applied to cDNAs from a near-isogenic pair of race T (Tox1+) and race O (Tox1-) strains. This led to discovery of PKS2, a second PKS-encoding gene that maps at Tox1A and is required for both Ttoxin biosynthesis and high virulence to maize. Thus, the carbon chain of each T-toxin family member likely is assembled by action of two PKSs, which produce two polyketides, one of which may act as the starter unit for biosynthesis of the mature T-toxin molecule.

scholarly journals A Decarboxylase Encoded at the Cochliobolus heterostrophus Translocation-Associated Tox1B Locus Is Required for Polyketide (T-toxin) Biosynthesis and High Virulence on T-cytoplasm Maize

2002 ◽  
Vol 15 (9) ◽  
pp. 883-893 ◽  
Author(s):  
Mark S. Rose ◽  
Sung-Hwan Yun ◽  
Thipa Asvarak ◽  
Shun-Wen Lu ◽  
O. C. Yoder ◽  
...  
Keyword(s):  
Polyketide Synthase ◽  
Pathogenic Fungus ◽  
Toxin Production ◽  
Cochliobolus Heterostrophus ◽  
Wild Type ◽  
Targeted Disruption ◽  
Transfer Event ◽  
High Virulence ◽  
Genes Encoding ◽  
Encoding Genes

Genes at two unlinked loci (Tox1A and Tox1B) are required for production of the polyketide T-toxin by Cochliobolus heterostrophus race T, a pathogenic fungus that requires T-toxin for high virulence to maize with T-cytoplasm. Previous work indicated that Tox1A encodes a polyketide synthase (PKS1) required for T-toxin biosynthesis and for high virulence. To identify genes at Tox1B, a wild-type race T cDNA library was screened for genes missing in the genome of a Tox1B deletion mutant. The library was probed, first with a 415-kb NotI restriction fragment from the genome of the Tox1B¯ mutant, then with the corresponding 560-kb fragment from the genome of wild type. Two genes, DEC1 (similar to aceto-acetate decarboxylase-encoding genes) and RED1 (similar to genes encoding members of the medium-chain dehydro-genase/reductase superfamily), were recovered. Targeted disruption of DEC1 drastically reduced both T-toxin production and virulence of race T to T-cytoplasm maize, whereas specific inactivation of RED1 had no apparent effect on T-toxin production (as determined by bioassay) or on virulence. DEC1 and RED1 map within 1.5 kb of each other on Tox1B chromosome 6;12 and are unique to the genome of race T, an observation consistent with the hypothesis that these genes were acquired by C. heterostrophus via a horizontal transfer event.

scholarly journals Cosegregation of Single Genes Associated with Fertility Restoration and Transcript Processing of Sorghum Mitochondrial orf107 and urf209

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 383-391 ◽  
Author(s):  
Hoang V Tang ◽  
Ruying Chang ◽  
Daryl R Pring
Keyword(s):  
Fertility Restoration ◽  
Mitochondrial Gene ◽  
Pollen Viability ◽  
Single Gene ◽  
Dominant Gene ◽  
Nuclear Gene ◽  
Male Sterile ◽  
Reading Frame ◽  
Transcript Processing ◽  
Backcross Populations

Abstract Defective nuclear-cytoplasmic interactions leading to aberrant microgametogenesis in sorghum carrying the IS1112C male-sterile cytoplasm occur very late in pollen maturation. Amelioration of this condition, the restoration of pollen viability, involves a novel two-gene gametophytic system, wherein genes designated Rf3 and Rf4 are required for viability of individual gametes. Rf3 is tightly linked to, or represents, a single gene that regulates a transcript processing activity that cleaves transcriptsof orf107, a chimeric mitochondrial open reading frame specific to IS1112C. The mitochondrial gene urf 209 is also subject to nucleus-specific enhanced transcript processing, 5′ to the gene, conferred by a single dominant gene designated Mmt1. Examinations of transcript patterns in F2 and two backcross populations indicated cosegregation of the augmented orf107 and urf209 processing activities in IS1112C. Several sorghum lines that do not restore fertility or confer orf107 transcript processing do exhibit urf209 transcript processing, indicating that the activities are distinguishable. We conclude that the nuclear gene(s) conferring enhanced orf107 and urf209 processing activities are tightly linked in IS1112C. Alternatively, the similarity in apparent regulatory action of the genes may indicate allelic differences wherein the IS1112C Rf3 allele may differ from alleles of maintainer lines by the capability to regulate both orf107 and urf209 processing activities.

scholarly journals Biochemical and molecular genetic analyses on placental aromatase (P-450AROM) deficiency.

1992 ◽  
Vol 267 (7) ◽  
pp. 4781-4785
Author(s):  
N Harada ◽  
H Ogawa ◽  
M Shozu ◽  
K Yamada ◽  
K Suhara ◽  
...  
Keyword(s):  
Molecular Genetic ◽  
Genetic Analyses

scholarly journals Molecular genetics of bipolar disorder

2001 ◽  
Vol 178 (S41) ◽  
pp. s128-s133 ◽  
Author(s):  
Nick Craddock ◽  
Ian Jones
Keyword(s):  
Bipolar Disorder ◽  
Candidate Gene ◽  
Molecular Genetics ◽  
Ethical Issues ◽  
Association Studies ◽  
Single Gene ◽  
Molecular Genetic ◽  
Genetic Dissection ◽  
Adoption Studies ◽  
Candidate Gene Association

BackgroundA robust body of evidence from family, twin and adoption studies demonstrates the importance of genes in the pathogenesis of bipolar disorder. Recent advances in molecular genetics have made it possible to identify these susceptibility genes.AimsTo present an overview for clinical psychiatrists.MethodReview of current molecular genetics approaches and emerging findings.ResultsOccasional families may exist in which a single gene plays a major role in determining susceptibility, but the majority of bipolar disorder involves more complex genetic mechanisms such as the interaction of multiple genes and environmental factors. Molecular genetic positional and candidate gene approaches are being used for the genetic dissection of bipolar disorder. No gene has yet been identified but promising findings are emerging. Regions of interest include chromosomes 4p16, 12q23–q24, 16p13, 21q22, and Xq24–q26. Candidate gene association studies are in progress but no robust positive findings have yet emerged.ConclusionIt is almost certain that over the next few years the identification of bipolar susceptiblity genes will have a major impact on our understanding of disease pathophysiology. This is likely to lead to major improvements and treatment in patient care, but will also raise important ethical issues.

scholarly journals Chromosomal anomalies that cause male sterility in the mouse also reduce ovary size

1984 ◽  
Vol 44 (2) ◽  
pp. 219-224 ◽  
Author(s):  
Ursula Mittwoch ◽  
Shantha Mahadevaiah ◽  
Leslie A. Setterfield
Keyword(s):  
Male Sterility ◽  
Germ Cells ◽  
Reciprocal Translocation ◽  
Chromosomal Anomalies ◽  
Male Sterile ◽  
Chromosome Anomalies ◽  
Ovarian Size ◽  
Males And Females ◽  
The Difference ◽  
Ovarian Involvement

SUMMARYTwo male-sterile chromosome anomalies, the insertion Is(7; 1)40H and the tertiary trisomy, Ts(512)31H, were found to be associated with reduced ovarian volumes in immature females. Together with the reciprocal translocation, T(11; 19)42H, in which this effect was described previously, reduced ovaries have been found in all three male-sterile chromosome anomalies investigated so far, suggesting that ovarian involvement is likely to be common in these conditions. Assuming that the smaller ovarian size reflects a reduction in the number of oocytes, it is suggested that male-sterile chromosome anomalies may exert basically similar deleterious effects on meiotic germ cells in males and females, the difference in outcome being due to cell-physiological differences between spermatocytes and oocytes and to the small number of surviving oocytes required for fertility in females.

scholarly journals Mosaic Trisomy 7 at Amniocentesis: Prenatal Diagnosis and Molecular Genetic Analyses

2010 ◽  
Vol 49 (3) ◽  
pp. 333-340 ◽  
Author(s):  
Chih-Ping Chen ◽  
Yi-Ning Su ◽  
Schu-Rern Chern ◽  
Yuh-Ming Hwu ◽  
Shuan-Pei Lin ◽  
...  
Keyword(s):  
Prenatal Diagnosis ◽  
Molecular Genetic ◽  
Genetic Analyses ◽  
Trisomy 7 ◽  
Mosaic Trisomy

Epigenetics and Applied Anthropology

2021 ◽  
Author(s):  
Charles H. Klein
Keyword(s):  
Social Inequalities ◽  
Homo Sapiens ◽  
Single Gene ◽  
Molecular Genetic ◽  
Healthcare Providers ◽  
Basic Research ◽  
Sufficient Information ◽  
Theoretical Frameworks ◽  
Noncoding Dna ◽  
Wide Range

Since Francis Crick and James D. Watson’s discovery of DNA in 1953, researchers, policymakers, and the general public have sought to understand the ways in which genetics shapes human lives. A milestone in these efforts was the completion of the Human Genome Project’s (HGP) sequencing of Homo sapiens’ nearly three million base pairs in 2003. Yet, despite the excitement surrounding the HGP and the discovery of the structural genetic underpinnings of several debilitating diseases, the vast majority of human health outcomes have not been linked to a single gene. Moreover, even when genes have been associated with particular diseases (e.g., breast and colon cancer), it is not well understood why certain genetically predisposed individuals become ill and others do not. Nor has the HGP’s map provided sufficient information to understand the actual functioning of the human genetic code, including the role of noncoding DNA (“junk DNA”) in regulating molecular genetic processes. In response, a growing number of scientists have shifted their attention from structural genetics to epigenetics, the study of how genes express themselves in particular situations and environments. Anthropologists play roles in these applications of epigenetics to real-world settings. Their new theoretical frameworks unsettle the nature-versus-nurture binary and support biocultural anthropological research demonstrating how race becomes biology and embodies social inequalities and health disparities across generations. Ethnographically grounded case studies further highlight the diverse epigenetic logics held by healthcare providers, researchers, and patient communities and how these translations of scientific knowledge shape medical practice and basic research. The growing field of environmental epigenetics also offers a wide range of options for students and practitioners interested in applying the anthropological toolkit in epigenetics-related work.

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