A selfish genetic element confers non-Mendelian inheritance in rice

Life is built on cooperation between genes, which makes it vulnerable to parasitism. Selfish genetic elements that exploit this cooperation can achieve large fitness gains by increasing their transmission relative to the rest of the genome. This leads to counter-adaptations that generate unique selection pressures on the selfish genetic element. This arms race is similar to host–parasite coevolution, as some multi-host parasites alter the host’s behaviour to increase the chance of transmission to the next host. Here, we ask if, similarly to these parasites, a selfish genetic element in house mice, the t haplotype, also manipulates host behaviour, specifically the host’s migration propensity. Variants of the t that manipulate migration propensity could increase in fitness in a meta-population. We show that juvenile mice carrying the t haplotype were more likely to emigrate from and were more often found as migrants within a long-term free-living house mouse population. This result may have applied relevance as the t has been proposed as a basis for artificial gene drive systems for use in population control.

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The t haplotype, a selfish genetic element, manipulates migration propensity in free-living wild house mice Mus musculus domesticus

10.1101/271247 ◽

2018 ◽

Author(s):

Jan-Niklas Runge ◽

Anna K. Lindholm

Keyword(s):

Population Control ◽

House Mice ◽

Gene Drive ◽

Genetic Element ◽

Mus Musculus Domesticus ◽

Free Living ◽

Mouse Population ◽

Selfish Genetic Elements ◽

Selfish Genetic Element ◽

Migration Propensity

AbstractLife is built on cooperation between genes, which makes it vulnerable to parasitism. However, selfish genetic elements that exploit this cooperation can achieve large fitness gains by increasing their transmission unfairly relative to the rest of the genome. This leads to counter-adaptations that generate unique selection pressures on the selfish genetic element. This arms race is similar to host-parasite co-evolution. Some multi-host parasites alter the host’s behaviour to increase the chance of transmission to the next host. Here we ask if, similarly to these parasites, a selfish genetic element in house mice, the t haplotype, also manipulates host behaviour, specifically the host’s migration propensity. Variants of the t that manipulate migration propensity could increase in fitness in a meta-population. We show that juvenile mice carrying the t haplotype were more likely to emigrate from and were more often found as migrants within a long-term free-living house mouse population. This result may have applied relevance as the t has been proposed as a basis for artificial gene drive systems for use in population control.

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Faculty Opinions recommendation of A synthetic maternal-effect selfish genetic element drives population replacement in Drosophila.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1074763.544855 ◽

2007 ◽

Author(s):

Steve Hedrick

Keyword(s):

Maternal Effect ◽

Genetic Element ◽

Population Replacement ◽

Selfish Genetic Element

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Independent evolution of tetraloop in enterovirus oriL replicative element and its putative binding partners in protein 3C

10.7287/peerj.preprints.3153v2 ◽

2017 ◽

Author(s):

Maria A Prostova ◽

Andrei A Deviatkin ◽

Irina O Tcelykh ◽

Alexander N Lukashev ◽

Anatoly P Gmyl

Keyword(s):

Amino Acid ◽

Genome Stability ◽

Rna Binding ◽

Apical Region ◽

Reading Frame ◽

Loop Region ◽

Binding Partners ◽

D Loop ◽

The One ◽

Species Specific

Background. Enteroviruses are small non-enveloped viruses with (+) ssRNA genome with one open reading frame. Enterovirus protein 3C (or 3CD for some species) binds the replicative element oriL to initiate replication. The replication of enteroviruses features low fidelity, which allows the virus to adapt to the changing environment on the one hand, and requires additional mechanisms to maintain the genome stability on the other. Structural disturbances in the apical region of oriL domain d can be compensated by amino acid substitutions in positions 154 or 156 of 3C (amino acid numeration corresponds to poliovirus 3C), thus suggesting the co-evolution of these interacting sequences in nature. The aim of this work was to understand co-evolution patterns of two interacting replication machinery elements in enteroviruses, the apical region of oriL domain d and its putative binding partners in the 3C protein. Methods.To evaluate the variability of the domain d loop sequence we retrieved all available full enterovirus sequences (>6400 nucleotides), which were present in the NCBI database on February 2017 and analysed the variety and abundance of sequences in domain d of the replicative element oriL and in the protein 3C. Results.A total of 2,842 full genome sequences was analysed. The majority of domain d apical loops were tetraloops, which belonged to consensus YNHG (Y=U/C, N=any nucleotide, H=A/C/U). The putative RNA-binding tripeptide 154-156 (Enterovirus C 3C protein numeration) was less diverse than the apical domain d loop region and, in contrast to it, was species-specific. Discussion. Despite the suggestion that the RNA-binding tripeptide interacts with the apical region of domain d, they evolve independently in nature. Together, our data indicate the plastic evolution of both interplayers of 3C-oriL recognition.

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Independent evolution of tetraloop in enterovirus oriL replicative element and its putative binding partners in protein 3C

10.7287/peerj.preprints.3153 ◽

2017 ◽

Author(s):

Maria A Prostova ◽

Andrei A Deviatkin ◽

Irina O Tcelykh ◽

Alexander N Lukashev ◽

Anatoly P Gmyl

Keyword(s):

Amino Acid ◽

Genome Stability ◽

Rna Binding ◽

Apical Region ◽

Reading Frame ◽

Loop Region ◽

Binding Partners ◽

D Loop ◽

The One ◽

Species Specific

Background. Enteroviruses are small non-enveloped viruses with (+) ssRNA genome with one open reading frame. Enterovirus protein 3C (or 3CD for some species) binds the replicative element oriL to initiate replication. The replication of enteroviruses features low fidelity, which allows the virus to adapt to the changing environment on the one hand, and requires additional mechanisms to maintain the genome stability on the other. Structural disturbances in the apical region of oriL domain d can be compensated by amino acid substitutions in positions 154 or 156 of 3C (amino acid numeration corresponds to poliovirus 3C), thus suggesting the co-evolution of these interacting sequences in nature. The aim of this work was to understand co-evolution patterns of two interacting replication machinery elements in enteroviruses, the apical region of oriL domain d and its putative binding partners in the 3C protein. Methods.To evaluate the variability of the domain d loop sequence we retrieved all available full enterovirus sequences (>6400 nucleotides), which were present in the NCBI database on February 2017 and analysed the variety and abundance of sequences in domain d of the replicative element oriL and in the protein 3C. Results.A total of 2,842 full genome sequences was analysed. The majority of domain d apical loops were tetraloops, which belonged to consensus YNHG (Y=U/C, N=any nucleotide, H=A/C/U). The putative RNA-binding tripeptide 154-156 (Enterovirus C 3C protein numeration) was less diverse than the apical domain d loop region and, in contrast to it, was species-specific. Discussion. Despite the suggestion that the RNA-binding tripeptide interacts with the apical region of domain d, they evolve independently in nature. Together, our data indicate the plastic evolution of both interplayers of 3C-oriL recognition.

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The maternal-effect, selfish genetic element Medea is associated with a composite Tc1 transposon

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.0800444105 ◽

2008 ◽

Vol 105 (29) ◽

pp. 10085-10089 ◽

Cited By ~ 34

Author(s):

M. D. Lorenzen ◽

A. Gnirke ◽

J. Margolis ◽

J. Garnes ◽

M. Campbell ◽

...

Keyword(s):

Maternal Effect ◽

Genetic Element ◽

Selfish Genetic Element

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Organization of the Plasmid cpe Locus in Clostridium perfringens Type A Isolates

Infection and Immunity ◽

10.1128/iai.70.8.4261-4272.2002 ◽

2002 ◽

Vol 70 (8) ◽

pp. 4261-4272 ◽

Cited By ~ 51

Author(s):

Kazuaki Miyamoto ◽

Ganes Chakrabarti ◽

Yosiharu Morino ◽

Bruce A. McClane

Keyword(s):

Clostridium Perfringens ◽

Horizontal Transfer ◽

Food Poisoning ◽

Type A ◽

Gastrointestinal Diseases ◽

Open Reading Frame ◽

Enterotoxin Gene ◽

Genetic Element ◽

Reading Frame ◽

Food Borne

ABSTRACT Clostridium perfringens type A isolates causing food poisoning have a chromosomal enterotoxin gene (cpe), while C. perfringens type A isolates responsible for non-food-borne human gastrointestinal diseases carry a plasmid cpe gene. In the present study, the plasmid cpe locus of the type A non-food-borne-disease isolate F4969 was sequenced to design primers and probes for comparative PCR and Southern blot studies of the cpe locus in other type A isolates. Those analyses determined that the region upstream of the plasmid cpe gene is highly conserved among type A isolates carrying a cpe plasmid. The organization of the type A plasmid cpe locus was also found to be unique, as it contains IS1469 sequences located similarly to those in the chromosomal cpe locus but lacks the IS1470 sequences found upstream of IS1469 in the chromosomal cpe locus. Instead of those upstream IS1470 sequences, a partial open reading frame potentially encoding cytosine methylase (dcm) was identified upstream of IS1469 in the plasmid cpe locus of all type A isolates tested. Similar dcm sequences were also detected in several cpe-negative C. perfringens isolates carrying plasmids but not in type A isolates carrying a chromosomal cpe gene. Contrary to previous reports, sequences homologous to IS1470, rather than IS1151, were found downstream of the plasmid cpe gene in most type A isolates tested. Those IS1470-like sequences reside in about the same position but are oppositely oriented and defective relative to the IS1470 sequences found downstream of the chromosomal cpe gene. Collectively, these and previous results suggest that the cpe plasmid of many type A isolates originated from integration of a cpe-containing genetic element near the dcm sequences of a C. perfringens plasmid. The similarity of the plasmid cpe locus in many type A isolates is consistent with horizontal transfer of a common cpe plasmid among C. perfringens type A strains.

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