Sex-linked gene traffic underlies the acquisition of sexually dimorphic UV color vision in Heliconius butterflies.
Sex-linked gene traffic underlies the acquisition of sexually dimorphic UV color vision in Heliconius butterflies.
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DOI：
10.1073/pnas.2301411120
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发表时间：
2023-08-15
影响因子：
11.1
通讯作者：
Briscoe, Adriana D.
中科院分区：
文献类型：
--
作者：
Chakraborty, Mahul;Lara, Angelica Guadalupe;Dang, Andrew;McCulloch, Kyle J.;Rainbow, Dylan;Carter, David;Ngo, Luna Thanh;Solares, Edwin;Said, Iskander;Corbett-Detig, Russell B.;Gilbert, Lawrence E.;Emerson, J. J.;Briscoe, Adriana D.
两性之间的差异是如何产生和进化的，这是进化生物学的一个中心问题。然而，由于大多数行为背后的神经回路的复杂性以及从全基因组序列数据重建完整染色体的困难，确定新行为特征的遗传起源已被证明是难以捉摸的。在这里，我们确定了一个这样的遗传机制，负责在蝴蝶属Heliconius的紫外线（紫外线）色觉的性二型性视蛋白基因的常染色体易位。我们发现，这种性二态行为的起源是不能很好地解释现有的模型。这代表了第一个已知的例子，性别有限的紫外线色觉在动物中，由于一个单一的基因移动到性染色体。新的性二态特征的获得提出了一个进化难题：新的特征是如何产生并成为性别限制的？最近获得的色觉，在灵长类和蝴蝶等动物中具有性别二态性，为理解性状如何成为性别偏见提供了一个令人信服的模型。例如，一些Heliconius蝴蝶独特地拥有UV（紫外线）色觉，这与两种差异调谐的UV敏感视紫红质UVRh1和UVRh2的表达相关。为了发现这些特征如何变得性二态，我们研究了Heliconius charithonia，它表现出女性特异性UVRh1表达。我们证明，女性，而不是男性，歧视不同的紫外线波长。通过全基因组鸟枪法测序和组装H。在charithonia基因组中，我们发现UVRh1存在于W染色体上，使其具有专性雌性特异性。通过敲除UVRh1，我们发现UVRh1蛋白表达在突变的女性眼组织中是不存在的，在野生型男性的眼睛。UVRh1性别连锁的PCR调查表明，具有雌性特异性UVRh1表达的物种在雄性中缺乏UVRh1 gDNA。因此，收购的性连锁是足以实现女性特异性表达的UVRh1，虽然这并不排除其他机制，如顺式调节进化也作出贡献。此外，这一事件以及导致差异UV视蛋白敏感性的突变都发生在Heliconius历史的早期。这些结果提出了一种不同于现有机制模型的获得性二态性的途径。我们提出了一个模型，基因交通的异源体（W或Y）遗传分区的性状性别表型转移（光谱调谐的紫外线敏感性）之前。
How differences between the sexes arise and evolve is a central question in evolutionary biology. However, identifying the genetic origins of new behavioral traits has proven elusive due to the complexity of the neural circuitry underlying most behaviors and the difficulty in reconstructing complete chromosomes from whole-genome sequence data. Here, we identify one such genetic mechanism responsible for sexual dimorphism in UV (ultraviolet) color vision in the butterfly genus Heliconius—an autosomal-to-sex chromosome translocation of an opsin gene. We find that the origins of this sexually dimorphic behavior are not well explained by existing models. This represents the first known example of sex-limited UV color vision in animals due to the movement of a single gene to a sex chromosome. The acquisition of novel sexually dimorphic traits poses an evolutionary puzzle: How do new traits arise and become sex-limited? Recently acquired color vision, sexually dimorphic in animals like primates and butterflies, presents a compelling model for understanding how traits become sex-biased. For example, some Heliconius butterflies uniquely possess UV (ultraviolet) color vision, which correlates with the expression of two differentially tuned UV-sensitive rhodopsins, UVRh1 and UVRh2. To discover how such traits become sexually dimorphic, we studied Heliconius charithonia, which exhibits female-specific UVRh1 expression. We demonstrate that females, but not males, discriminate different UV wavelengths. Through whole-genome shotgun sequencing and assembly of the H. charithonia genome, we discovered that UVRh1 is present on the W chromosome, making it obligately female-specific. By knocking out UVRh1, we show that UVRh1 protein expression is absent in mutant female eye tissue, as in wild-type male eyes. A PCR survey of UVRh1 sex-linkage across the genus shows that species with female-specific UVRh1 expression lack UVRh1 gDNA in males. Thus, acquisition of sex linkage is sufficient to achieve female-specific expression of UVRh1, though this does not preclude other mechanisms, like cis-regulatory evolution from also contributing. Moreover, both this event, and mutations leading to differential UV opsin sensitivity, occurred early in the history of Heliconius. These results suggest a path for acquiring sexual dimorphism distinct from existing mechanistic models. We propose a model where gene traffic to heterosomes (the W or the Y) genetically partitions a trait by sex before a phenotype shifts (spectral tuning of UV sensitivity).
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影响因子：
64.8
作者：
Dasmahapatra, Kanchon K.;Walters, James R.;Briscoe, Adriana D.;Davey, John W.;Whibley, Annabel;Nadeau, Nicola J.;Zimin, Aleksey V.;Hughes, Daniel S. T.;Ferguson, Laura C.;Martin, Simon H.;Salazar, Camilo;Lewis, James J.;Adler, Sebastian;Ahn, Seung-Joon;Baker, Dean A.;Baxter, Simon W.;Chamberlain, Nicola L.;Chauhan, Ritika;Counterman, Brian A.;Dalmay, Tamas;Gilbert, Lawrence E.;Gordon, Karl;Heckel, David G.;Hines, Heather M.;Hoff, Katharina J.;Holland, Peter W. H.;Jacquin-Joly, Emmanuelle;Jiggins, Francis M.;Jones, Robert T.;Kapan, Durrell D.;Kersey, Paul;Lamas, Gerardo;Lawson, Daniel;Mapleson, Daniel;Maroja, Luana S.;Martin, Arnaud;Moxon, Simon;Palmer, William J.;Papa, Riccardo;Papanicolaou, Alexie;Pauchet, Yannick;Ray, David A.;Rosser, Neil;Salzberg, Steven L.;Supple, Megan A.;Surridge, Alison;Tenger-Trolander, Ayse;Vogel, Heiko;Wilkinson, Paul A.;Wilson, Derek;Yorke, James A.;Yuan, Furong;Balmuth, Alexi L.;Eland, Cathlene;Gharbi, Karim;Thomson, Marian;Gibbs, Richard A.;Han, Yi;Jayaseelan, Joy C.;Kovar, Christie;Mathew, Tittu;Muzny, Donna M.;Ongeri, Fiona;Pu, Ling-Ling;Qu, Jiaxin;Thornton, Rebecca L.;Worley, Kim C.;Wu, Yuan-Qing;Linares, Mauricio;Blaxter, Mark L.;Ffrench-Constant, Richard H.;Joron, Mathieu;Kronforst, Marcus R.;Mullen, Sean P.;Reed, Robert D.;Scherer, Steven E.;Richards, Stephen;Mallet, James;McMillan, W. Owen;Jiggins, Chris D.
通讯作者：
Jiggins, Chris D.
DOI：
10.1534/g3.115.023655
发表时间：
2016-01-15
期刊：
G3 (Bethesda, Md.)
影响因子：
--
作者：
Davey JW;Chouteau M;Barker SL;Maroja L;Baxter SW;Simpson F;Merrill RM;Joron M;Mallet J;Dasmahapatra KK;Jiggins CD
通讯作者：
Jiggins CD
影响因子：
3.3
作者：
Chang, Ching-Ho;Larracuente, Amanda M.
通讯作者：
Larracuente, Amanda M.
影响因子：
3.3
作者：
Catalan, Ana;Briscoe, Adriana D.;Hohna, Sebastian
通讯作者：
Hohna, Sebastian
影响因子：
48
作者：
Chin, Chen-Shan;Peluso, Paul;Schatz, Michael C.
通讯作者：
Schatz, Michael C.