Homologous recombination changes the context of Cytochrome b transcription in the mitochondrial genome of Silene vulgaris KRA

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61389030%3A_____%2F18%3A00498480" target="_blank" >RIV/61389030:_____/18:00498480 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.1186/s12864-018-5254-0" target="_blank" >http://dx.doi.org/10.1186/s12864-018-5254-0</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1186/s12864-018-5254-0" target="_blank" >10.1186/s12864-018-5254-0</a>

Result language

angličtina

Original language name

Homologous recombination changes the context of Cytochrome b transcription in the mitochondrial genome of Silene vulgaris KRA

Original language description

Background: Silene vulgaris (bladder campion) is a gynodioecious species existing as two genders male-sterile females and hermaphrodites. Cytoplasmic male sterility (CMS) is generally encoded by mitochondrial genes, which interact with nuclear fertility restorer genes. Mitochondrial genomes of this species vary in DNA sequence, gene order and gene content. Multiple CMS genes are expected to exist in S. vulgaris, but little is known about their molecular identity. Results: We assembled the complete mitochondrial genome from the haplotype KRA of S. vulgaris. It consists of five chromosomes, two of which recombine with each other. Two small non-recombining chromosomes exist in linear, supercoiled and relaxed circle forms. We compared the mitochondrial transcriptomes from females and hermaphrodites and confirmed the differentially expressed chimeric gene bobt as the strongest CMS candidate gene in S. vulgaris KRA. The chimeric gene bobt is co-transcribed with the Cytochrome b (cob) gene in some genomic configurations. The co-transcription of a CMS factor with an essential gene may constrain transcription inhibition as a mechanism for fertility restoration because of the need to maintain appropriate production of the necessary protein. Homologous recombination places the gene cob outside the control of bobt, which allows for the suppression of the CMS gene by the fertility restorer genes. We found the loss of three editing sites in the KRA mitochondrial genome and identified four sites with highly distinct editing rates between KRA and another S. vulgaris haplotypes (KOV). Three of these highly differentially edited sites were located in the transport membrane protein B (mttB) gene. They resulted in differences in MttB protein sequences between haplotypes. Conclusions: Frequent homologous recombination events that are widespread in plant mitochondrial genomes may change chromosomal configurations and also the control of gene transcription including CMS gene expression. Posttranscriptional processes, e.g. RNA editing shall be evaluated in evolutionary and co-evolutionary studies of mitochondrial genes, because they may change protein composition despite the sequence identity of the respective genes. The investigation of natural populations of wild species such as S. vulgaris are necessary to reveal important aspects of CMS missed in domesticated crops, the traditional focus of the CMS studies.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

10609 - Biochemical research methods

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2018

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

BMC Genomics

ISSN

1471-2164

e-ISSN

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Volume of the periodical

19

Issue of the periodical within the volume

DEC 4

Country of publishing house

US - UNITED STATES

Number of pages

17

Pages from-to

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UT code for WoS article

000452123100002

EID of the result in the Scopus database

2-s2.0-85057998090