New genes often acquire male-specific functions but rarely become essential in <i>Drosophila</i>

Kondo, Shu; Vedanayagam, Jeffrey; Mohammed, Jaaved; Eizadshenass, Sogol; Kan, Lijuan; Pang, nan sim; Aradhya, Rajaguru; Siepel, Adam; Steinhauer, Josefa; Lai, Eric C.

doi:10.1101/gad.303131.117

Cited by 70 publications

(112 citation statements)

References 29 publications

(48 reference statements)

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“…Last, I investigated the functional outcomes of gene duplication and deletion in Drosophila by comparing expression profiles introduced by gene duplication to those lost by gene deletion. Consistent with previous studies in Drosophila (Betrán et al 2002;Dai et al 2006;Assis and Bachtrog 2013;Assis 2014;Zhao et al 2014;Kondo et al 2017;Rogers et al 2017), child duplicates created by gene duplication are often testis-expressed. However, I found that testis-expressed genes are lost by deletion just as frequently as they are gained by duplication, indicating that their deletion rates are perhaps driven solely by their frequencies in the genome.…”

Section: Discussionsupporting

confidence: 88%

“…; Kondo et al. ; Rogers et al. ), child duplicates created by gene duplication are often testis‐expressed.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies in Drosophila (Betrán et al 2002;Dai et al 2006;Assis and Bachtrog 2013;Assis 2014;Zhao et al 2014;Kondo et al 2017;Rogers et al 2017) and mammals (Marques et al 2005;Vinckenbosch et al 2006) have demonstrated that gene duplication alters the gene expression landscape by generating child copies that are primarily expressed in the testis. This phenomenon may occur because transcription in the testis is more promiscuous than in other tissues due to open chromatin states during meiosis and less stringent promoter requirements (Kaessmann 2010).…”

Section: By Gene Duplication and Deletionmentioning

confidence: 99%

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Out of the testis, into the ovary: biased outcomes of gene duplication and deletion in Drosophila

Assis

2019

Evolution

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Gene turnover is a key source of adaptive variation. Yet most evolutionary studies have focused on gene duplication, dismissing gene deletion as a mechanism that simply eradicates redundancy. Here, I use genome‐scale sequence and multi‐tissue expression data from Drosophila melanogaster and Drosophila pseudoobscura to simultaneously assess the evolutionary outcomes of gene duplication and deletion in Drosophila. I find that gene duplication is more frequent than gene deletion in both species, indicating that it may play a more important role in Drosophila evolution. However, examination of several genic properties reveals that genes likely possess distinct functions after duplication that diverge further before deletion, suggesting that loss of redundancy cannot explain a majority of gene deletion events in Drosophila. Moreover, in addition to providing support for the well‐known “out of the testis” origin of young duplicate genes, analyses of gene expression profiles uncover a preferential bias against deletion of old ovary‐expressed genes. Therefore, I propose a novel “into the ovary” hypothesis for gene deletion in Drosophila, in which gene deletion may promote adaptation by salvaging genes that contribute to the evolution of female reproductive phenotypes. Under this combined “out of the testis, into the ovary” evolutionary model, gene duplication and deletion work in concert to generate and maintain a balanced repertoire of genes that promote sex‐specific adaptation in Drosophila.

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Section: Discussionsupporting

confidence: 88%

“…; Kondo et al. ; Rogers et al. ), child duplicates created by gene duplication are often testis‐expressed.…”

Section: Discussionmentioning

confidence: 99%

Section: By Gene Duplication and Deletionmentioning

confidence: 99%

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Out of the testis, into the ovary: biased outcomes of gene duplication and deletion in Drosophila

Assis

2019

Evolution

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“…Because CRISPR/Cas9 generates targeted double-stranded breaks in DNA, this technique can be used to create both "knock-out" mutations, via imprecise repair of Cas9-induced lesions via the non-homologous endjoining pathway (NHEJ), as well as "knock-in" mutations, where an exogenously-supplied DNA donor serves as a template for homology-directed repair (HDR) (Gratz et al 2014). Indeed, a number of genome-wide Drosophila collections are currently being generated for both knock-outs (Kondo et al 2017), and knock-ins (e.g. Lee et al 2018).…”

Section: Introductionmentioning

confidence: 99%

ovo^Dco-selection: a method for enriching CRISPR/Cas9-edited alleles inDrosophila

Ewen-Campen

Perrimon

2018

Preprint

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Screening for successful CRISPR/Cas9 editing events remains a time consuming technical bottleneck in the field of Drosophila genome editing. This step can be particularly laborious for events that do not cause a visible phenotype, or those which occur at relatively low frequency. A promising strategy to enrich for desired CRISPR events is to co-select for an independent CRISPR event that produces an easily detectable phenotype. Here, we describe a simple negative co-selection strategy involving CRISPR-editing of a dominant female sterile allele, ovo D1 . In this system ("ovo D co-selection"), the only functional germ cells in injected females are those that have been edited at the ovo D1 locus, and thus 100% of the offspring of these flies have undergone editing of at least one locus. We demonstrate that ovo D co-selection can be used to enrich for knock-out mutagenesis via nonhomologous end-joining (NHEJ), and for knock-in alleles via homology-directed repair (HDR).Altogether, our results demonstrate that ovoD co-selection reduces the amount of screening necessary to isolate desired CRISPR events in Drosophila.

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“…We do not understand the function of either the non-coding RNA or the testis specific hts variant, but the presence of these transcripts hints at the complex evolutionary history of this gene and its regulation in both the male and female germline. Although the germline is permissive for the evolution of new genes or new gene functions, recent CRISPR-mediated mutagenesis of a subset of recently evolved genes determined that very few new genes are essential for fertility and none of those tested were essential for viability (Kondo et al 2017).…”

Section: Htsrc Evolution and Fecunditymentioning

confidence: 99%

HtsRC-mediated accumulation of F-actin regulates ring canal size during Drosophila melanogaster oogenesis

Gerdes

Mannix

Hudson

et al. 2020

Preprint

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Ring canals in the female germline of Drosophila melanogaster are supported by a robust filamentous actin (F-actin) cytoskeleton, setting them apart from ring canals in other species and tissues. Previous work has identified components required for the expansion of the ring canal actin cytoskeleton but has not identified the proteins responsible for F-actin recruitment or accumulation. Using a combination of CRISPR-Cas9 mediated mutagenesis and UAS-Gal4 overexpression, we show that HtsRC, a component specific to female germline ring canals, is both necessary and sufficient to drive F-actin accumulation. Absence of HtsRC in the germline resulted in ring canals lacking inner rim F-actin, while overexpression of HtsRC led to larger ring canals. HtsRC functions in combination with Filamin to recruit F-actin to ring-canal-like ectopic actin structures in somatic follicle cells. Finally, we present findings which indicate that HtsRC expression and robust female germline ring canal expansion are important for high fecundity in fruit flies but dispensable for their fertility, a result which is consistent with our understanding of HtsRC as a newly evolved gene specific to female germline ring canals.

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New genes often acquire male-specific functions but rarely become essential in Drosophila

Cited by 70 publications

References 29 publications

Out of the testis, into the ovary: biased outcomes of gene duplication and deletion in Drosophila

Out of the testis, into the ovary: biased outcomes of gene duplication and deletion in Drosophila

ovo^Dco-selection: a method for enriching CRISPR/Cas9-edited alleles inDrosophila

HtsRC-mediated accumulation of F-actin regulates ring canal size during Drosophila melanogaster oogenesis

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New genes often acquire male-specific functions but rarely become essential in Drosophila

Cited by 70 publications

References 29 publications

Out of the testis, into the ovary: biased outcomes of gene duplication and deletion in Drosophila

Out of the testis, into the ovary: biased outcomes of gene duplication and deletion in Drosophila

ovoDco-selection: a method for enriching CRISPR/Cas9-edited alleles inDrosophila

HtsRC-mediated accumulation of F-actin regulates ring canal size during Drosophila melanogaster oogenesis

Contact Info

Product

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ovo^Dco-selection: a method for enriching CRISPR/Cas9-edited alleles inDrosophila