1. Human Mitochondrial Genetics - Wikipedia, The Free Encyclopedia mitochondrial genetics is the study of the genetics of the DNA contained in mitochondria. Mitochondria are small structures in cells that generate energy http://en.wikipedia.org/wiki/Human_mitochondrial_genetics

Human mitochondrial genetics From Wikipedia, the free encyclopedia Jump to: navigation search Contents Mitochondrial function and genome Membrane complexes Genome Genetic code variants ... Sources Mitochondrial genetics is the study of the genetics of the DNA contained in mitochondria . Mitochondria are small structures in cells that generate energy for the cell to use, and are hence referred to as the "powerhouses" of the cell. Mitochondrial DNA (mtDNA) is not transmitted through nuclear DNA (nDNA), and in most multicellular organisms, virtually all mitochondria are inherited from the mother's ovum , as sperm cells do not contribute any mitochondria. Mitochondrial inheritance is therefore non-Mendelian , as Mendelian inheritance presumes that half the genetic material of a fertilized egg ( zygote ) derives from each parent. Eighty percent of mitochondrial DNA codes for functional mitochondrial proteins, and therefore most mitochondrial DNA mutations lead to functional problems, which may be manifested as muscle disorders ( myopathies Understanding the genetic mutations that affect mitochondria can help us to understand the inner workings of cells and organisms, as well as helping to suggest methods for successful therapeutic tissue and organ cloning, and to treatments or possibly cures for many devastating muscular disorders.

2. Mitochondrial Genetics mitochondrial genetics is peculiar and complex because mitochondrial DNA is maternally inherited and can be present at tens to tens of thousands of copies http://www.wormbook.org/chapters/www_mitogenetics/mitogenetics.html

Embryo series courtesy of Einhard Schierenberg Home About WormBook Author Instructions Sponsors ... WormBase HTML Preprints PDF Download PDF version Mitochondrial genetics Bernard Lemire Department of Biochemistry, University of Alberta, Edmonton, Alberta, T6G 2H7 Canada This chapter is in WormBook section: > Genetics and genomics >> Genomics Table of Contents 1. Introduction 2. Mitochondrial DNA structure 3. mtDNA-encoded proteins 4. Mitochondrial DNA inheritance ... 12. References Abstract The mitochondrial genome is vital for Caenorhabditis elegans metabolism, physiology, and development. The C. elegans 1. Introduction The mitochondrial genome is indispensable to the cellular and organismal biology of Caenorhabditis elegans . An elaborate cellular machinery is employed to maintain mitochondrial DNA (mtDNA), to express it, and to ensure its inheritance. Because it is maternally transmitted and because of its wide-ranging copy number (it can be present at fewer than 100 to tens of thousands of copies per cell), the genetics of mtDNA are characterized by a number of peculiar and as yet incompletely understood features. The fundamental importance of mtDNA to cellular energy metabolism explains the profound effects mtDNA mutations can have; mitochondria are the major source of reactive oxygen species, which are implicated in premature aging and senescence.

3. Mitochondrial Genetics Laboratory Mitochondrial iron homeostasis is vital for OXPHOS maintenance and antioxidant protection. Both the heme and iron-sulfur cluster biosynthetic pathways http://mayoresearch.mayo.edu/mayo/research/isayalab/

Appointments Jobs About Search ... Home personnel Faculty and Staff current projects Mitochondrial Oxidative Phosphorylation more pages Lab Photos Selected Publications Research Highlights Our research centers on the mechanisms that enable the cell to take advantage of the high energetic yield of oxidative phosphorylation (OXPHOS) in spite of the concomitant production of reactive oxygen species (ROS). Defects in these mechanisms lead to energy depletion and oxidative damage, which are increasingly implicated in degenerative disease and aging. Mitochondrial iron homeostasis is vital for OXPHOS maintenance and anti-oxidant protection. Both the heme and iron-sulfur cluster biosynthetic pathways depend on a constant supply of iron to the mitochondrial matrix, where micromolar concentrations of iron must be kept in reduced, available, and non-toxic form. This is a formidable challenge for the cell because the superoxide anion and hydrogen peroxide produced by the respiratory chain favor the iron-catalyzed production of the highly toxic hydroxyl radical. Friedreich ataxia (FRDA) provides a dramatic example of what happens when mitochondria lose their ability to process iron properly. FRDA (

4. CiteULike: Mitochondrial Genetics Of Aging: Intergenomic Conflict Resolution keywords = {aging, genetics, mitochondria}, month = {November}, number = {45}, pages = {re5+}, priority = {0}, title = {mitochondrial genetics of Aging http://www.citeulike.org/user/kristen/article/2253048

Register Log in FAQ CiteULike News Discussion Journals Browse current issues Groups Search groups CiteULike is a free online bibliography manager. Register and you can start organising your references online. Library Groups Watchlist Profile ... Import Mitochondrial Genetics of Aging: Intergenomic Conflict Resolution by: David M Rand Sci. Aging Knowl. Environ. , Vol. 2005, No. 45. (9 November 2005), re5. Plain APA Chicago Elsevier Harvard IEEE MLA Nature Oxford Science Turabian Vancouver View FullText article DOI Pubmed Hubmed Find related articles from these CiteULike users kristen Find related articles with these CiteULike tags aging genetics mitochondria Abstract Mitochondria are the organelles of aerobic respiration. They consume the oxygen we breathe to stay alive and generate energy for cells to function. But oxygen can be dangerous. Indeed, mitochondria generate the majority of reactive oxygen species that are prime suspects among the causes of aging. Mitochondria have been influential elements of evolving eukaryotic cells for perhaps 2 billion years, since a eubacterium fused with an archaebacterium. The picture that has emerged from this long history of genomic fusion is that of a complex network of nuclear-mitochondrial cross-talk. Here, we discuss the biochemical and genetic conflicts between mitochondria and nucleus, which have shaped the role of mitochondria in aging, and point to new paths for further investigations. 10.1126/sageke.2005.45.re5 BibTeX record EndNote BibTeX kristen's tags All tags in kristen's library

5. Modified Recombination And Transmission Of Mitochondrial Genetic Markers In Rho mitochondrial genetics. IV. Allelism and mapping studies of oligomycin resistant mutants in S. cerevisiae. Mol Gen Genet. 1973 Sep 5;125(1)9–52. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=431565

6. Mitochondrial DNA Mutations In Human Disease : Abstract : Nature Reviews Genetic The human mitochondrial genome is extremely small compared with the nuclear genome, and mitochondrial genetics presents unique clinical and experimental http://www.nature.com/nrg/journal/v6/n5/abs/nrg1606.html

Jump to main content Jump to navigation nature.com homepage ... Login Search This journal All of Nature.com Advanced search Journal home Archive Review Abstract Review Nature Reviews Genetics (May 2005) doi Mitochondrial DNA mutations in human disease Robert W. Taylor About the authors Top of page Abstract The human mitochondrial genome is extremely small compared with the nuclear genome, and mitochondrial genetics presents unique clinical and experimental challenges. Despite the diminutive size of the mitochondrial genome, mitochondrial DNA (mtDNA) mutations are an important cause of inherited disease. Recent years have witnessed considerable progress in understanding basic mitochondrial genetics and the relationship between inherited mutations and disease phenotypes, and in identifying acquired mtDNA mutations in both ageing and cancer. However, many challenges remain, including the prevention and treatment of these diseases. This review explores the advances that have been made and the areas in which future progress is likely. View At a Glance Top of page Author affiliations Mitochondrial Research Group, School of Neurology, Neurobiology and Psychiatry, The Medical School, University of Newcastle upon Tyne, NE2 4HH, United Kingdom.

7. Mitochondrial Inheritance And Hearing Loss - Genetics And Deafness - Information This article will give a short introduction to mitochondrial genetics, and outline the spectrum of clinical presentations of mitochondrially determined http://www.boystownhospital.org/Hearing/info/genetics/concepts/mito.asp

@import "/css/complex.css"; This site was designed for more recent browsers, but it is accessible to any browser or Internet device. To view the site correctly please update your browser. Click here for a list of more recent browsers. More than 24,000 children are born with hearing loss in the United States each year. Boys Town National Research Hospital is a national leader in the diagnosis and treatment of children with moderate to profound hearing loss. @import "/css/rightcol.css"; What's New How to Find Us Contact Us Pediatrics ... Donate by Mail Information on Hearing Loss - Genetics and Deafness - Mitochondrial Inheritance and Hearing Loss by Nathan Fischel-Ghodsian, M.D. Nearly all of our genes can be found in the nucleus of the cell on one of the 23 chromosome pairs. However there are other genes on the tiny chromosomes in the mitochondria of the cell. Recently, mutations in these mitochondrial chromsomes have been found to be associated with a variety of hearing defects. This article will give a short introduction to mitochondrial genetics, and outline the spectrum of clinical presentations of mitochondrially determined hearing impairments. Normal Mitochondrial Genetics Mitochondrial DNA is transmitted exclusively through mothers, with sperm apparently contributing no mitochondrial DNA to the zygote. This leads to the expectation that a defect in a mitochondrial gene should lead to disease equally in both sexes, but can only be transmitted through the maternal line. These basic rules of mitochondrial genetics are complicated by at least four factors:

8. Mitochondrial Genetics Of Aging: Intergenomic Conflict Resolution -- Rand 2005 ( Citation D. M. Rand, mitochondrial genetics of Aging Intergenomic Conflict Resolution. Sci. Aging Knowl. Environ. 2005 (45), re5 (2005). http://sageke.sciencemag.org/cgi/content/abstract/2005/45/re5

Science 's SAGE KE Jump to: Page Content Section Navigation Site Navigation Site Search ... Account Information , or Site Tools Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be. Site Tools Site Search Site Area Science Magazine Daily News Science Signaling SAGE KE Science Careers All HighWire Journals Terms Advanced Account Information Guest Alerts Access Rights My Account Sign In Site Navigation Readers Members Authors Librarians Advertisers Issue Archive Community Resources Highlights ... Reviews Article Views Abstract Full Text (HTML) Full Text (PDF) E-Letters Article Tools Download Citation Post to CiteULike Request Permission To Use This Article View PubMed Citation Related Content Similar Articles In: SAGE KE PubMed Search Google Scholar for: Articles by Rand, D. M. Search PubMed for: Articles by Rand, D. M.

9. LTU: Microbiology: Dictyostelium Mitochondrial Genetics Laboratory Dr Christian Barth and the Dictyostelium mitochondrial genetics Laboratory. http://www.latrobe.edu.au/microbiology/barth.html

La Trobe Home Skip to Content Contact the Department Sitemap ... Our Research Mitochondrial Genetics Our Staff Seminars Site Map Web Links Dr. Christian Barth Welcome to the Dictyostelium Mitochondrial Genetics Page Dr. Christian Barth is a lecturer in the Department of Microbiology at La Trobe University, Melbourne, Australia Location: Mitochondrial Genetics Laboratory Department of Microbiology La Trobe University, Victoria, 3086 AUSTRALIA Contact Information: Office Phone: Lab Phone: Fax: E-mail: C.Barth@latrobe.edu.au Research Interests: Mitochondria are found in almost all eukaryotic cells. They are the powerhouse of the cell, generating energy in form of ATP, and have other important functions in haem and lipid biosynthesis, intracellular signal transduction and programmed cell death. According to the endosymbiotic hypothesis Although the number of proteins still encoded in the mitochondrial genome is relatively small, the organellar genome has to be maintained, replicated and transcribed, and the encoded gene products have to be synthesised on ribosomes in the mitochondrial matrix. The genetic processes involved are quite different from those in the nucleus and in the cytoplasm of the eukaryotic host - in fact they are strikingly similar to the genetic processes found in bacteria. However, the proteins that mediate mitochondrial replication, transcription and protein synthesis are now all nuclear-encoded.

10. Mitochondria, Genetics Studies on patients with these diseases have revealed much about the complexities of mitochondrial genetics, which involves an interplay between mutations http://lib.bioinfo.pl/meid:980

Favored by Comments Papers 2165 (rec: 0) Reports Pending Editor: PubMed Papers Reports Books Mesh-terms Authors Users username: password: Register Forgot password Login Register to comment articles, reports and participate in mesh term forums Register to monitor favorite articles, reports, mesh-terms, authors, users Register to publish reports in the BioInfoBank Library and become editor Register to create Your own user record to promote Your scientific activity Mitochondria , genetics Latest Paper: Med Sci (Paris). 2007 May ;23 (5):519-25 17502069 [Targeting allotopic material to the mitochondrial compartment: new tools for better understanding mitochondrial physiology and prospect for therapy] [My paper] Pierre Rustin Howard T Jacobs Andr© Dietrich Robert N Lightowlers ... Marisol Corral-Debrinski Mitochondrial disorders can not be ignored anymore in most medical areas. They include specific and widespread organ involvement, with tissue degeneration or tumor formation, being the target of numerous viruses, e.g. the HIV. Primary or secondary actors, mitochondrial dysfunctions are also supposedly playing a role in the ageing process. Despite the progresses made in the identification of their molecular bases, nearly all remains to be done as regards therapy. Research dealing with mitochondrial physiology and pathology has a long history in France and is thus not a surprise if four French teams, coming from these fundamental domains, are involved in the challenge to find ways to fight these diseases. The directions described are working tracks which promise to be long and full of pitfalls. Being original, they share a part of risk and uncertainty, but they are also with great potential with high stakes if considering the impact of these diseases.

11. ScienceDirect - Trends In Genetics : Mitochondrial DNA – All Things Bad? In any rapidly growing area of research, such as mitochondrial genetics, there will inevitably be areas of controversy. Perhaps the most emotive issue in http://linkinghub.elsevier.com/retrieve/pii/S0168952598016849

Athens/Institution Login Not Registered? User Name: Password: Remember me on this computer Forgotten password? Home Browse My Settings ... Help Quick Search Title, abstract, keywords Author e.g. j s smith Journal/book title Volume Issue Page Trends in Genetics Volume 15, Issue 3 , 1 March 1999, Pages 91-93 Abstract Full Text + Links PDF (384 K) Related Articles in ScienceDirect Ageing and mammalian mitochondrial genetics Trends in Genetics Ageing and mammalian mitochondrial genetics Trends in Genetics Volume 14, Issue 12 1 December 1998 Pages 513-517 Phillip Nagley and Yau-Huei Wei Abstract Abstract Full Text + Links PDF (216 K) Mitochondrial mutagenesis in the brain in forensic and ... ... Legal Medicine Mitochondrial mutagenesis in the brain in forensic and pathological research Legal Medicine Volume 5, Issue 1 March 2003 Pages 1-6 Nicole von Wurmb-Schwark, Thorsten Schwark, Christoph Meissner and Manfred Oehmichen Abstract Accumulation of alterations to the mitochondrial DNA (mtDNA) would be expected to significantly impair the bioenergetic function of mitochondria in the affected host cells. Many of these changes have been associated with several specific diseases and the process of aging. These mutations may be the result of mitochondrial oxidative stress, which is increased with age of individuals and specific degenerative diseases. Our aim with this review is to summarize the recent literature on the occurrence of mtDNA alterations and its possible relation to age-depending degenerative processes with special regards to the brain. Additionally, we show how these alterations could be used in fields of pathology and forensic medicine.

12. Mitochondrial Genetics - EvoWiki Mitochondrial genetic mutations that occur in the nuclear DNA can occur in any of the chromosomes (depending on the species). http://wiki.cotch.net/index.php/Mitochondrial_genetics

Mitochondrial genetics From EvoWiki Jump to: navigation search In genetics, Mitochondria are the powerhouses of the cell, producing ATP through the metabolism of pyruvic acid and other energy containing molecules. They also help detoxify the cell by catabolic processes in which they breakdown fatty and amino acids Contents Why It Is Important Mitochondrial Membrane Complexes Mitochondrial Genome Detailed Inheritance Patterns of Mitochondrial Diseases ... edit Why It Is Important Having a greater understanding of the genetic mutations which affect mitochondria can not only give us a much better understanding of how our bodies and cells work, evolution, and give us insight into methods for successful therapeutic tissue and organ cloning, but it can also lead us to better treatments and possibly even cures for many of the diseases that devastate many individuals and families. edit Mitochondrial Membrane Complexes The processes carried out by the electron transport chain are mediated by protein complexes (named Complexes I-V, DHO-QO, ETF-QO, and ANT). Complex I, or NADH dehydrogenase ubiquinone oxidoreductase , uses the energy in NADH and uses to pump protons into the intermembrane space of the mitochondrion, pumping 4 protons per electron and passing energy on to complex III (coenzyme Q or ubiquinone:Cytochrome bc1 oxidoreductase) in the form of an electron. Complex II (succinate:CoQ Oxidoreductase) accepts energy from FADH2 produced in the

13. Mitochondrial Genetics And Hearing Loss: The Missing Link Between Genotype And P mitochondrial genetics and hearing loss the missing link between genotype and phenotype. N FischelGhodsian Ahmanson Department of Pediatrics, http://www.ebmonline.org/cgi/content/abstract/218/1/1

HOME HELP FEEDBACK SUBSCRIPTIONS ... TABLE OF CONTENTS QUICK SEARCH: [advanced] Author: Keyword(s): Year: Vol: Page: This Article Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Fischel-Ghodsian, N. Search for Related Content PubMed PubMed Citation Articles by Fischel-Ghodsian, N. MINIREVIEWS Mitochondrial genetics and hearing loss: the missing link between genotype and phenotype N Fischel-Ghodsian Ahmanson Department of Pediatrics, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, California 90048, USA. nfischel@mailgate.csmc.edu Mitochondrial DNA mutations have been implicated in a great variety of diseases, including such common ones as diabetes, Parkinson's disease and Alzheimer's, but the pathophysiological pathway leading from a specific

14. Clinical Mitochondrial Genetics -- Chinnery Et Al. 36 (6): 425 -- Journal Of Med Clinical mitochondrial genetics. Patrick F Chinnerya, Neil Howellb, Richard M Andrewsa c, Douglass M Turnbulla. a Department of Neurology, The University of http://jmg.bmjjournals.com/cgi/content/abstract/36/6/425

HOME HELP FEEDBACK SUBSCRIPTIONS ... REGISTER Author Keyword(s) Vol Page [Advanced] This Article Full Text Full Text (PDF) Submit a response ... Citation Map Services Email this link to a friend Similar articles in this journal Similar articles in PubMed Add article to my folders ... Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chinnery, P. F Articles by Turnbull, D. M Search for Related Content PubMed PubMed Citation Articles by Chinnery, P. F Articles by Turnbull, D. M Related Collections Genetics J Med Genet 425-436 ( June ) Review article Clinical mitochondrial genetics Patrick F Chinnery a Neil Howell b Richard M Andrews a c Douglass M Turnbull a a Department of Neurology, The University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, UK, b Department of Radiation Oncology, University of Texas Medical Branch, Galveston, Texas, USA, c Department of Ophthalmology, The University of Newcastle upon Tyne, UK Correspondence to: Dr Chinnery.

15. IngentaConnect Mitochondrial Genetics And Disease mitochondrial genetics and disease. Author Schon E.A.. Source Trends in Biochemical Sciences, Volume 25, Number 11, 1 November 2000 , pp. 555560(6) http://www.ingentaconnect.com/content/els/09680004/2000/00000025/00000011/art016

var tcdacmd="dt"; Home About Ingenta Ingenta Labs Ingenta Blog ... Check our FAQs Or contact us to report problems with: Subscription access Article delivery Registration Library administrator tasks ... Other problems For Publishers Why go online? Why choose IngentaConnect? Beyond Print: enhancing your service Access and authentication ... Contact us For Researchers For Authors About IngentaConnect Search and browse Publications available ... Register For Librarians Resource Zone Why choose IngentaConnect? Why choose IngentaConnect Complete? Activating Subscriptions ... Register CM8ShowAd("HorizontalBanner"); Mitochondrial genetics and disease Author: Schon E.A. Source: Trends in Biochemical Sciences , Volume 25, Number 11, 1 November 2000 , pp. 555-560(6) Publisher: Elsevier view table of contents Key: - Free Content - New Content - Subscribed Content - Free Trial Content CM8ShowAd("Skyscraper"); Language: English Document Type: Review article DOI: This article is hosted on another website. You may be required to register, activate a subscription or purchase the article before you can obtain the full text.

16. Mitochondrial Genetics Of Emphasis Type= Italic Coprinus Your browser may not have a PDF reader available. Google recommends visiting our text version of this document. http://www.springerlink.com/index/G743707427855315.pdf

17. Polarity And Suppressiveness Mitochondrial Genetics In Bakers Your browser may not have a PDF reader available. Google recommends visiting our text version of this document. http://www.pnas.org/cgi/reprint/71/11/4612.pdf?ref=Yapma.net?ref=Yapma.net

18. ARS | Publication Request: UNIQUE MITOCHONDRIAL GENETICS OF CUCUMIS Unique mitochondrial genetics of cucumis Abstract. Plant and Animal Genome Abstracts. Available http//www.intlpag.org/14/abstracts/PAG14_W76.html. http://www.ars.usda.gov/research/publications/Publications.htm?seq_no_115=188041

19. NeuroCAST - Genetics And Diagnosis Of Mitochondrial Disorders This article is a brief review of mitochondrial genetics, disorders, and their diagnosis for neurologists, geneticists, genetic counselors, http://www.neurocast.com/site/content/sessions_02_2002.asp

Mitochondria are the intracellular organelles that supply most of a cell's energy needs by producing adenosine triphosphate (ATP) through oxidative phosphorylation. More recently, mitochondria have also been found to play a central role in programmed cell death, or apoptosis. In addition to these well-known tasks, mitochondria are also responsible for a variety of other metabolic functions specific to the almost 250 different cell types in the human body. Mitochondria are unique organelles in that they contain their own DNA (mtDNA), which is distinct from the DNA in the cell nucleus (nDNA). Thus, proper mitochondrial function depends on the coordinated expression of both the nuclear and mitochondrial genomes and therefore, mitochondrial dysfunction can arise from mutations in either genome (Figure 1). This article is a brief review of mitochondrial genetics, disorders, and their diagnosis for neurologists, geneticists, genetic counselors, and other healthcare professionals involved in the care of people with complex neurological diseases that may be due to mitochondrial dysfunction. Figure 1.

20. Epsilon Dissertations And Graduate Theses Archive - Mitochondrial Genetics Of Al Leino, Matti (2005) mitochondrial genetics of alloplasmic malesterile Brassica napus lines. Doctoral diss. Dept. of Plant Biology and Forest Genetics, SLU. http://diss-epsilon.slu.se/archive/00000801/

@import url(http://epsilon.slu.se/eprints.css); @import url(http://epsilon.slu.se/diss_eprints.css); @import url(http://epsilon.slu.se/eprints.css); @import url(http://epsilon.slu.se/diss_eprints.css); @import url(http://epsilon.slu.se/print.css); Epsilon - electronic publishing at the SLU SLU Libraries Epsilon Dissertations and Graduate Theses Archive Home Browse Search Publish ... Contact Mitochondrial genetics of alloplasmic male-sterile Brassica napus lines Leino, Matti Mitochondrial genetics of alloplasmic male-sterile Brassica napus lines Doctoral diss Dept. of Plant Biology and Forest Genetics SLU Acta Universitatis agriculturae Sueciae vol. Full text available as: PDF 2241 Kb Abstract Reliable and economical production of hybrid (F1) varieties requires efficient means to control pollination. The predominant system for pollination control of most field crops today is cytoplasmic male sterility (CMS). Since CMS is a consequence of disturbed nuclear-mitochondrial interactions, the CMS trait is maternally inherited. A common way to produce CMS plants is to combine the nuclear genome from one species with the mitochondria from another; plants of such origin are described as alloplasmic CMS. This thesis describes the production and molecular characterization of a novel alloplasmic CMS system produced from rapeseed (Brassica napus) (+) Arabidopsis thaliana somatic hybrids. A population of 170 B. napus (+) A. thaliana somatic hybrid lines was backcrossed to B. napus and 22 lines with male sterility and/or aberrant flower morphology were found. Nine of these were analysed for RFLP and found to contain nuclear and plastid DNA from B. napus, whilst the mitochondrial genomes were frequently recombined containing both B. napus and A. thaliana DNA. Besides the male-sterile trait, the majority of the lines displayed homeotic conversions of anthers to carpeloid organs. Vegetative growth was reduced to some extent in some of the lines. One CMS line segregated both fertile and sterile plants. Fertility co-segregated with molecular markers from A. thaliana chr III. By a dihaploidisation strategy we produced plants with a disomic addition of A. thaliana chr III, which had a stable inheritance of the fertile phenotype.

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