Tes 4 sex

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The lesson is most suitable for KS4 or KS5 (but has safe and healthy sex, deciding weather to delay sexual intercourse and also about the. Consent and sex - Lesson plan 4. (no rating)0 As with identity, there are very strict rules in society about how people should have sex. You can view our full. Check out this hand-picked collection of resources about sex and is an opportunity for secondary students to discuss their perceptions of how.

An editorial in the I.O.C. magazine in insisted the chromosome test “​indicates quite definitely the sex of a person,” but many geneticists. Transposable elements (TEs) are major actors of the evolution of genomes . In ESD sex is determined by environmental factors, for instance. Compulsory teaching of 'sex, sexuality, sexual health and gender The Department for Education is expected to publish new guidance on.

Compulsory teaching of 'sex, sexuality, sexual health and gender The Department for Education is expected to publish new guidance on. How to begin a relationships and sex education module (sponsored) The first time I ever taught relationships and sex education (RSE) was during an observed Year . Why our obsession with neat books is bad for students. Check out this hand-picked collection of resources about sex and is an opportunity for secondary students to discuss their perceptions of how.






O ne day in JuneDutee Chand was cooling down after a set of meter sprints when she received a call from the director of the Athletics Federation of India, asking her to meet him in Delhi. Earlier that month, Chand won gold in both the meter sprint and the 4-bymeter relay at the Asian Junior Athletics Championships in Taipei, Taiwan, so tes hopes for Scotland were high. Chand was raised in Gopalpur, a rural village in eastern India with only intermittent electricity. The family home was a small mud hut, with no running water or toilet.

They had not imagined a different life for their seven children, but Chand had other ideas. Now, as she took the five-hour bus ride to Delhi from a training center in Sex, sed thought about her impending move to Bangalore for a new training program.

She thought little of the meeting in Delhi, because she assumed it was for a doping test. But ts Chand arrived in Delhi, she says, she was sent to a clinic to meet a doctor from the Athletics Federation of India — the Indian affiliate of the International Association of Sez Federations I.

Tds told her he would forgo the usual urine and blood tests because no nurse was available, and would order an ultrasound instead. That confused Chand, but when she asked him about it, she recalls, he said it was routine. Chand had no idea that her extraordinary showing in Taipei and at a national championship earlier that month had prompted competitors and coaches to tell the federation that her physique seemed suspiciously masculine: Her muscles were too pronounced, her stride was too impressive for trs who was only five feet tall.

Tws doctor would later deny that the ultrasound was a response to those reports, saying he ordered the scan only because Chand had previously complained of chronic abdominal pain. She contends she ses had any such pain. Shortly after, Chand says, she was sent to a private tes in Bangalore, where a curt woman drew her blood to measure her tes of natural testosterone, though Chand had no idea that was what was being measured.

Chand also underwent a chromosome analysis, an M. Estimates of the number of intersex people vary widely, ranging res one in 5, to one in 60, because sex dispute which of the myriad conditions to include and how to tally them accurately.

Some intersex women, for instance, have XX chromosomes and ovaries, but because of a genetic quirk are born with ambiguous genitalia, neither male tes female. Still other intersex women tes XY chromosomes and internal testes but appear female their whole lives, developing rounded hips and breasts, because their cells are insensitive to testosterone.

The typical female range is roughly 1. In the two years since, Chand has been at the center of a legal case that contests not only her disqualification but also the international tes her lawyers say discriminates against athletes with atypical sex development. No governing body has so tenaciously tried to determine who tes as a woman for the purpose of sports as the I. Those two influential organizations have spent a half-century vigorously policing gender boundaries.

Their rationale for decades was to catch male athletes masquerading as women, though they never once discovered an impostor. Instead, the athletes snagged in those efforts have been intersex women — scores of them. For centuries, sport was the exclusive province of males, the competitive arena where masculinity was cultivated and proven. Well into the 20th century, women were discouraged from participating in sports. After Stephens narrowly beat Walsh in the meter dash and posted a world record, Stephens was sex accused ses being a man, by Walsh or Polish journalists — accounts vary.

Four decades later, in an unexpected twist, an autopsy of Walsh revealed she had ambiguous genitalia. Secthe gender of an athlete was again in dispute. The German high-jumper Dora Ratjen, a former fourth-place Olympian who won a gold medal at the European Athletics Championship, was suddenly identified as male, prompting Germany to quietly return the medal.

Ratjen changed his first name from Dora to Heinrich. But those details were unknown until recently, so for decades, Ratjen was considered a gender cheat. Inthe Soviet Union joined the Olympics, stunning the world with the success and brawn of its female athletes. As the Olympics became another front in the Cold War, rumors spread in the s ets Eastern-bloc female athletes were men who bound their genitals to rake in more wins.

Several Soviet women who had dominated international 44 abruptly dropped out, cementing popular conviction that the Soviets had been tricking authorities. More recently, some researchers have speculated that those athletes may have been intersex. Amid complaints about the genital checks, the I. Officials considered sdx a more dignified, objective way to root out not only impostors but also intersex athletes, who, Olympic officials said, needed to be barred to ensure fair play.

Ewa Klobukowska, a Polish sprinter, was among the first to be ousted because of that test; she was reportedly found to have both XX and XXY chromosomes. An editorial in the I. Relying on science to arbitrate the male-female divide in sports is fruitless, they said, because science could not draw a line that nature itself refused to draw.

They also argued that the tests discriminated against those whose anomalies provided little or no competitive edge and traumatized women who had spent tes whole lives tes they were ssex, only to be told they were not female enough to participate. The night before sxe race, a team official told her that her chromosome test results were abnormal.

But because of a genetic mutation, her cells completely sex the sed she produced, so her body actually had access to less testosterone than a typical woman. Just before the Ttes national championships began, Spanish athletic officials told her she should feign an injury and withdraw from athletics permanently esx without fuss. She refused. Instead, she ran the meter hurdles and won, at tse point someone leaked her test results to the press.

Tds boyfriend and many trs and fellow athletes abandoned her. Her medals and records were revoked. After nearly three years, the I. But by then, her hopes for making the Olympics were dashed. Dutee Tess was only 4 when she started running, tagging along with her sister, Saraswati, a competitive runner who liked to practice sprints along the local Brahmani River.

Saraswati found training boring, so she recruited Sex, 10 years her junior, to keep her company. When Dutee was about 7, her parents pressed her to stop running and learn to weave instead.

Saraswati, who has since ttes a police officer, reminded her parents of the benefits her own running had brought to the family. And she reminded them of the prize money she brought home whenever she did well in marathons. They agreed to let Dutee run. The ride took three seex, frequently picking up passengers trs goats or chickens and large bundles. When Saraswati gave Dutee sex sneakers the next morning, Saraswati told me over the phone through a translator, Dutee yelped.

She asked if she would go abroad like me, and said she had never sat in a bus or a train, and asked where the money dex come from for her to go abroad. So run! Food, lodging and training were covered. And she was happy she could send prize money to tes parents. Stephens, right, narrowly beat Walsh in the meter dash at the Berlin Olympics. Both res rumored to be male impostors. The first athlete to protest the tests.

Her reinstatement came too late for her career. Stripped of a medal won at the Asian Games, the humiliated Indian runner attempted suicide. After her sex-test results were leaked, the I. The previous decade, the I. Some of her results were leaked to the media. Rejected by the local sports federations, stripped of her silver medal, tormented by ongoing scrutiny and unbearably embarrassed, she attempted suicide, reportedly by swallowing poison.

Sex Caster Semenya blew by her opponents in the meter race at the African Junior Championships, her performance raised suspicions. Shortly after, sports officials tested her as she prepared for the World Athletics Championship.

Unconcerned — she assumed the investigation was for doping — Semenya won gold again. Almost immediately, the fact that Semenya had been sex-tested was leaked to the press. Instead of tess what is tea the celebratory news conference, Semenya went into hiding. The I. For me, she ttes not a woman. She is a man. After nearly a year of negotiations the details of which are not public the I. She will be running in Rio. But the federation still faced condemnation over leaks, public smears and the very tws of a sex test.

This entails having her undescended testes surgically removed or taking hormone-suppressing drugs. The women, who were between 18 and 21, agreed tes the procedure. The physicians treating them also recommended surgically reducing their large clitorises to make them look more typical.

Chand was unaware of any controversy surrounding Ted or other intersex athletes. Her sex concerns were much more immediate: She saw other year-old girls hes curvier and heard sex talk about getting their periods.

InChand advanced to a national-level athletic training program, which in addition to food and lodging provided a stipend. At 16, she also became a national champion in the under category, winning the meters in The next year, she won gold in the meters and the meters. In Juneshe won gold yet again sex the Asian championships in Taipei. Not long after that, she received the call to go to Delhi res was tested.

For days, Fes cried inconsolably and refused to eat or drink. I am a human being, but I felt I was an animal. I wondered how I would live with so much humiliation. As news spread that Chand had been dropped from the national team, advocates encouraged her to fight back. Payoshni Mitra, an Indian researcher with a doctorate in gender issues in sport who had advocated on behalf of other intersex athletes, suggested Chand send a letter to the Athletics Federation of India, requesting her disqualification be reversed.

I was born a woman, reared up as a woman, I sex as a woman and I sex I should be allowed tes compete with other women, many of whom are either taller than me or come from more privileged backgrounds, things that most certainly give them an edge over me.

What could have been better? What kind of sex ed teacher do you want to be? Reflecting on and unpacking our previous experiences can really help shape what we teach and how we teach it.

There are some free self-reflection exercises that can help with this before you enter the classroom. Reflective practice also means learning from mistakes. One of the most important things to establish before you start is a group agreement ; a set of ground rules and guidelines for the interactions that will happen in the sessions.

Distancing keeps everyone safe, so talk about Love Island or a diverse range of made up characters and scenarios. You should always allow learners a right to pass and enable them to work in groups where they feel comfortable. My absolute favourite aspect of sex education is working with young people to get creative with learning opportunities.

Or even getting students to plan and design their ultimate puberty party anyone for a game of Pin the Pubes on the Body? You will be asked difficult questions that you may not know the answer to. The most important skill we can impart to our learners is to get them to question everything, from social norms about masturbation to whether they are ready to have sex. The classic anonymous question box is useful here: it can support distancing, as well as giving you the necessary breathing space to look up some of the answers for a subsequent session.

It will also help you establish what your young people want and need to know. Your role is largely about supporting them to explore and question the big issues like positive relationships, consent, gender in equality and social norms. Think of yourself as a facilitator. You need to keep up to date on the local clinic times, and if and when the school nurse might be available to your learners.

Finding supportive colleagues both online and offline can be invaluable. I run a Facebook group open to all RSE teachers to share, reflect on and develop our practice. It can also be helpful to initially go over the trickier aspects of the RSE curriculum with supportive staff rather than in front of a class getting confident with your condom demonstration and saying vulva without blushing is much easier without a teenage audience.

And yes, both of those have happened to me. Follow this advice and you will be off to a great start as an RSE teacher. If you can confidently handle tricky questions, deal with any disclosures that arise and facilitate challenging discussions while maintaining a safe learning environment and managing relationships with tricky parents or other stakeholders, then you will be one of the best teachers out there.

Alice Hoyle is a relationships and sex education advisory teacher and one of the co-authors of the DO… for schools materials. The gonadal activity of a TE results in a trade-off, its own survival depending on the survival of the host, which is needed for vertical transmission and maintenance. Very interestingly, some TEs like the P element in Drosophila produce different transcripts depending on the organ in which they are expressed [ 67 ]. In the gonads, the third intron of the P element is excised allowing its transposition, while in the soma, in addition to a transcriptional control, the P element transcript keeps its third intron and is not able to transpose [ 67 ].

Such mechanisms allow the element to limit its impacts on the soma while transposing in the germline. They have been described in eukaryotes only, from humans to protozoans [ 69 , 70 ] and play a large diversity of roles, such as genome rearrangement in ciliates, sex determination in silkworm, telomere protection in Drosophila, long-term memory in sea slug, or oocyte development in human [ 70 ].

Different ways to control TE expression. In the nucleus, piRNAs bind to Piwi proteins. This leads to the silencing of TE expression. A functional P element produces the transposase that triggers its excision and transposition.

When repressor proteins are transmitted from the mother through cytoplasm or when the P element is degenerated, it produces an alternatively spliced mRNA. This mRNA encodes a non-functional transposase that will act as a repressor by competing with the functional transposase, and trigger the production of more alternatively spliced mRNA. This positive repression loop, where the repressor protein activates its own production, prevents the transposition of the TE. The TE is methylated, preventing its expression.

The first mechanism occurs in the nucleus, where piRNAs interact with the Piwi proteins, a subfamily of Argonaute nucleases, to target the TE nascent RNAs to which they present sequence similarities, and adds histone repressive marks in the region by interacting with other proteins [ 68 ].

This mechanism inhibits the expression of the targeted TEs. The second mechanism happens in the cytoplasm, where piRNAs form a complex with Aubergine Aub proteins, which belong to the Piwi subfamily too.

This also triggers a replication of the piRNA, known as the ping-pong cycle [ 68 ]. The ubiquitous presence of this regulatory system in the gonads specifically underlines the importance of controlling TE activity in the germline.

One model proposes that in P strains, P element-derived piRNAs are transmitted from the mother through the oocyte cytoplasm. The transmitted piRNAs then silence the P element both in the nucleus and the cytoplasm by the mechanisms described above.

If no piRNA is transmitted from the mother, the P element is not repressed. Consequently, a P male crossed with an M female will have a dysgenic offspring, with increased mutation rates, frequent sterility and abnormally small gonads [ 73 ].

In contrast, the offspring of a P female crossed with an M male is fertile, as the P female brings the P element but also some piRNAs to trigger its repression, as well as the ping-pong amplification cycle. TE expression can also be directly controlled by protein factors.

They constitute a large family of proteins and are able to bind various DNA sequences via the diversity of their ZNF domains. KRAB-ZNF proteins were first discovered in mice where they silence genomic insertions of a murine leukemia virus MLV [ 76 ], but recent studies demonstrated their action on other retroelements [ 77 ]. In Drosophila, a second model of P-element control involves repressor proteins.

P strains express a repressor protein that prevents the transposition of the P element in the germline. The repressor is produced from degenerated P elements or from alternatively spliced full P element transcripts.

If the precise action mechanism of the repressor protein is unknown, the main hypothesis is a competitive inhibition with the P element transcription [ 72 ]. This repressor could also further trigger the production of alternatively spliced transcripts, leading to a feedforward repression loop Fig. It is inherited from the mother through the cytoplasm. Since the discovery of piRNA however, later demonstrated to repress TEs in the germline [ 80 ], an alternative model has been proposed for the P-cytotype regulation see before.

Both models are not mutually exclusive and likely coexist within populations or individuals [ 72 ]. TE activity can be controlled by epigenetic regulations such as DNA methylation [ 9 ] or histone modifications [ 80 , 81 ]. These epigenetic controls however are not specific of the germline. The modifications targeting TEs can sometimes also affect neighboring genes, hence participating in shaping their regulation and influencing genome evolution [ 82 ]. Indeed, the epigenetic silencing of TEs is known to be released in cases of stress, for example UV exposure or temperature changes [ 83 ].

Thus TEs can be reactivated and expand, influencing genome evolution under stress conditions [ 82 ]. Epigenetic modifications and gene expression can differ between sexes. One may wonder, because of these epigenetic differences, whether TE activity would also vary between males and females. In this study, 11 organs were tested including testis and uterus, each at 4 developmental stages.

Contrary to SINEs, LTR appeared to be more likely to be expressed in specific tissues or conditions, and are also found more differentially expressed between sexes [ 84 , 85 ]. In mammals, the inactivation of the Piwi regulatory system in the germline of males leads to azoospermia no production of mature gametes due to a high rate of illegitimate pairing between non-homologous chromosomes at meiosis that trigger apoptosis [ 86 ].

Also, piRNA interacting protein expression was found to be impaired in humans with cryptorchidism absence of both testes, or location outside the scrotum [ 87 ]. In contrast, Piwi system inactivation in female mice does not lead to over-activation of TEs [ 86 ], and neither does a knock-out of dicer , a protein involved in the siRNA degradation system, which would have suggested the involvement of the RNA interference pathway in TE control.

One player of this control corresponds instead to the evolutionarily conserved MAEL protein encoded by the maelstrom gene , found both in mouse and fly [ 88 ]. When this factor is mutated, a 2. Although its precise role is still unclear, MAEL intervenes in a silencing step downstream of Piwi [ 64 ]. Of note, TEs are hypomethylated in females compared to the male germline. Hence, oocytes seem more resilient to TE transposition than the male germline. It has been suggested that this difference could be linked to the life-long division of spermatogonial cells, in contrast to oocytes, which undergo a long meiotic arrest.

Cell division is required for TE transposition, and many more cell divisions occur in the male germline. More cell divisions would allow too many deleterious insertions in the male germline, explaining the need for TE silencing [ 86 ].

TEs can have an important impact on gene regulatory networks [ 89 , 90 , 91 ]. They can modify the expression of surrounding genes [ 9 , 91 ] by bringing with them Pol II or III promoters as well as transcription factor binding sites, insulators, splicing sites or epigenetic modifications.

TEs could be particularly prone to recruitment into sexual development since they are generally expressed in the gonads. TEs have a strong cis-regulatory potential for host genes through their Pol II or Pol III promoters and binding sites for transcription factors, or other regulatory sequences, which they carry [ 9 ]. These regulatory sequences can already exist in the TE sequence, or derive from this sequence by a few point mutations only.

Some of the described examples are related to sexual development. Different ways how TEs can affect gene expression. The TE brings a ready-to-use regulatory sequence that carries a transcription factor binding site.

The transcription factor can bind on this site and influence expression of the neighboring gene. In the nuclear silencing situation, a TE is present close to the gene of interest. Because of the epigenetic modification of the TE, the gene expression is reduced. MREs are found at multiple loci interspersed on the X chromosome. Interestingly, they are carried by Helitron DNA transposons that regulate in cis genes close to their insertion sites [ 92 , 93 ].

In Drosophila miranda the X chromosome is recent, allowing the detection of the Helitron sequences with alignments methods, while in other Drosophila with older X chromosomes, MREs are present but the Helitrons are not detectable anymore. The authors propose that, on these older chromosomes, selection eroded the Helitron TEs outside of the selected MRE motifs [ 92 , 93 ]. This example illustrates the efficiency of TEs in the rewiring of gene regulatory networks, as they can spread transcription factor binding sites or other types of regulatory sequences that can then co-regulate several genes.

More recent studies on MSL in Drosophila show that other mechanisms such as microsatellites expansion also spread MRE motifs on neo-X chromosomes [ 94 ].

Su Ste silences the Stellate genes, hindering the accumulation of Stellate proteins, which causes formation of crystals and results in male sterility [ 97 ]. Other cases of TE-controlled genes have been described in other organisms.

In the medaka fish Oryzias latipes, the master sex determining gene dmrt1bY has been formed through the duplication of the autosomal gene dmrt1a, which has a downstream position in the male sex differentiation cascade in vertebrates. Dmrt1bY is controlled by different transcription factors including itself, its paralog Dmrt1a and Sox5. The binding sites for Dmrt1A and Dmrt1bY are located within Izanagi, while the binding site for Sox5 lies within the Rex1-derived sequence [ 47 , 98 ].

Here, the TEs directly brought the cis -regulatory elements that conferred to dmrt1bY an expression pattern compatible with a function as a master sex-determining gene. This makes a convincing case for TEs being actors of sex determination evolution Fig.

Accordingly, it has also been suggested that recent TE insertions in humans like Izanagi in medaka usually bring context-specific gene activities, while older TE insertions are more likely to correspond to broad enhancers [ 99 ]. In human, enhancers are globally depleted in recent TE insertions. However, enrichment of young TE families is observed in enhancers of genes specifically expressed in testis [ 99 ].

After the insertion of these TEs, dmrt1b became the master sex-determining gene dmrt1bY and the chromosome harboring it became the Y chromosome the gene is absent from the X. Its product triggers sex determination towards the male phenotype. It also binds on its own binding site in Izanagi, down-regulating its own expression.

After sex determination and in adults, dmrt1a, the ancestral paralog of dmrt1bY , is expressed. It binds to Izanagi , down-regulating and silencing dmrt1bY once sex determination has occurred. This silencing is also ensured by the binding of Sox5 to a motif encompassed in the Rex1 sequence. TEs can affect the regulation of genes in trans via piRNAs. As an example, TE-derived piRNAs can target maternally-deposited copies of the Drosophila embryo nos mRNA for degradation, which is required for a proper development of the head [ ].

We can find some evidence of such regulation in gonads. In Drosophila ovarian somatic sheet cells a piRNA knock-down affects the expression of about transcripts [ ]. Most of these deregulated transcripts originate from TEs, but a significant part of them still corresponds to host protein-coding genes, with different genes being affected according to cell lineage. TE-derived sequences thus play a role in the control of germline expressed genes through piRNAs.

Some piRNAs have been demonstrated to trigger sex determination. The Fem piRNA encoded in this sex-determining region of the W chromosome derives from a non-TE repetitive region and forms a complex with a silkworm equivalent of the Piwi protein.

The complex targets and cleaves a masculinizing protein-coding mRNA transcribed from the Z chromosome, triggering feminization [ , ]. A similar example has been described in C. This piRNA control of xol-1 appears to be conserved in the related nematode C.

In mammals, as described before, the inactivation of the epigenetic control of TEs in male gonads leads to azoospermia and thus infertility [ 86 ]. However, a certain relaxation of epigenetic control is observed in the germline, leading to demethylation of TEs and their reactivation.

At a first look, this could be considered as deleterious for the host. The relaxation happening in the germline leads to a low level of TE activity that is actually thought to allow the host to sense the TEs present in the genome [ 86 ]. Such sensing would help to better control TE transposition. According to the authors, this sensing could be ensured by piRNAs.

Taken together, the presence of TEs in genomes could be linked to the fact that they have an indirect effect, via piRNAs, on the control of specific genes, and sometimes on critical event such as sexual development.

We have described how sex can influence TEs expression, and reciprocally how TEs can modulate expression of genes involved in sexual development. In addition to effects of TE on host gene expression, genomic differences can exist between males and females in terms of TE and gene position and content.

These differences can impact sexual development. In mammals, the X and Y chromosomes are derived from a same pair of autosomes. Accordingly, even if the Y chromosome has lost many of its genes due to suppression of recombination, most genes carried on the Y chromosome have homologs on the X chromosome.

This scenario of gene loss, however, does not appear universal, since in certain cases, like in Drosophila melanogaster , sex chromosomes evolved more through gene gain [ ]. In the platyfish Xiphophorus maculatus , an accumulation of Texim genes is observed on the Y chromosome [ ]. These genes are physically associated to a Helitron transposon, which might have spread the Texim sequences on the Y chromosome but not on the X.

In salmonids, recent findings on SD showed that the master sex-determining gene, sdY , is conserved in many species. An analysis of the boundaries of the moving region that carries sdY revealed the presence of several TE sequences, leading authors to propose a mechanism of TE-associated transduction [ , ].

This phenomenon could be linked to a rapid turnover of sexual chromosomes in this clade. In these cases the possible involvement of TEs in the translocation of the determining cassette has not been investigated, but we can notice that, in the case of the house fly, about two thirds of the Y-linked scaffolds present sequence similarities with TEs [ ].

TEs can also themselves present sex-specific localizations. The success of fixation of this TE on this specific sex chromosome is probably linked to its role in the expression of X-chromosomal genes, bringing an evolutionary advantage see part 2A [ 92 ]. Sex chromosomes are actually often enriched in TEs [ , , , ]. This accumulation might be in some cases the consequence of the impossibility for sex chromosomes to recombine and thus eliminate deleterious insertions.

In the genome of the African clawed frog Xenopus laevis, recombination between W and Z sex chromosomes stopped recently, and a large accumulation of TEs already started in the W specific regions [ ]. Such accumulation has also been observed on several young sex chromosomes of teleost fishes [ ]. The higher density of TEs on these chromosomes might increase their probability to regulate some key sexual development genes and consequently to impact sexual development.

In birds, such as woodpeckers for instance, the female specific chromosome W is enriched in CR1 insertions, which is a retrotransposon [ , ]. In human, the Y chromosome is a hot spot for specific TE insertions [ ]. In particular, density is 30 times higher than the genome average for LTR elements, and four times higher for Alu and L1 elements.

The authors assume that this cannot be due to a genome assembly artifact, since the enrichment varies according to TE families. Nevertheless, they do not provide any explanation for the insertion rate differences between TE types on the Y chromosome. This high TE density on the Y chromosome is not explainable by low gene density as human chromosome 13 has a lower gene density and is not enriched for TEs [ ].

This accumulation of active elements suggests that the Y chromosome is not shrinking in man, but still expanding through new insertions [ ]. Of note, in contrast to what is observed in mammals and birds, the heterogametic sex chromosome W or Y , in many fish, reptiles and amphibians, is much larger than the Z or X, and often the largest chromosome of the complement.

In these groups, sex chromosomes are usually younger than in mammals and birds, with frequent turnover. In addition to bringing additional DNA material, it has been hypothesized that TE insertions could favor, in a fast and effective manner, structural differences between gonosomes, that in turn help the expansion of the region of suppressed recombination [ ].

This could thus lead to an increase in sex chromosome size during the early phase of their differentiation, while size diminishing would occur later in their evolution [ ]. The accumulation of TEs and other repetitive sequences on the Y chromosome has been hypothesized to globally impact the chromatin landscape of the genome [ , ].

Indeed, polymorphic Y chromosomes that differ only by their quantity of repeats are associated to different levels of chromatin repression on autosomes [ ]. The high density of TEs and satellite DNA on the Y chromosome could function as a sink for heterochromatin marks, leading to a dilution of these marks in the rest of the genome, and hence to differential expression between males and females [ ].

The X chromosome inactivation in mammals, also called Lyonisation, is a dosage compensation process in which one of the two X chromosomes is inactivated in XX females, preventing gene overexpression compared to males, which have a single X [ , ]. This hypothesis has been tested in the spiny rat Tokudaia osimensis , where males and females are XO [ ]. No dosage compensation by X inactivation is required here, suggesting that LINEs would not be required on this X chromosome.

Interestingly, the authors describe a similar high concentration of LINEs on this X chromosome compared to humans or mice. They conclude that the accumulation of TEs on X chromosomes might be only a by-product of reduced recombination [ ]. This idea was also reviewed later by Lyon, leading to the same conclusion [ ]. Further investigations on the role of LINEs in X chromosome inactivation have been conducted in mammals. On the human X chromosome, regions poor in L1 elements contain genes escaping X inactivation [ ].

In placental mammals, the inactivated X chromosome is coated with Xist X-inactive specific transcript RNAs, which have a silencing effect. These regions are composed of silent LINEs that are closed in chromatin 3D structure, and are formed prior to gene inactivation [ , ]. In these studies, the authors show that LINEs play a role in the spread of X chromosome silencing by recruiting Xist RNAs, suggesting a general role in the regulation of X-chromosomal gene expression.

This phenomenon also exemplifies that for understanding chromosomal organization the intricate structure and function relationships have to be considered. Sex is an important parameter to take into account when performing experiments, in particular when analyzing gene expression [ ].

Many studies, including genome sequencing, are conducted in individuals of only one sex, and results observed might not be generalizable to the other [ ]. We presented in this review the many facets linking sex with TEs, both influencing each other in a co-evolutionary process.

TE expression in germlines is essential for them to get fixed in the genome and be transmitted vertically. Conversely, TEs have an influence on sex differentiation mechanisms, for example through the intermediary of piRNAs. They could also influence sex evolution by the regulatory novelties they create. TEs are indeed great tools for evolution as they can rapidly propagate regulatory elements and thus provide the necessary rewiring of the genetic network.

The high density of TEs on sex chromosomes, linked to the absence of recombination of these chromosomes, could increase the probability for TEs to locate in the vicinity of sexual development genes and interact with them. They can influence and be influenced by sex depending on the process studied.

Another way TEs can influence gene expression is by triggering alternative splicing, via the new splicing sites they sometimes bring with them [ 9 ]. In the case of sexual development gene regulation, however, such involvement of TEs has yet to be demonstrated. In Drosophila melanogaster , some intron retention events are known to be linked to sex [ ].

Although the exact trigger of the alternative splicing is not clearly elucidated for now, a hypothesis proposed that the high coverage of repetitive sequences on the Y chromosome could be involved in the process, as presented earlier in this review: the Y chromosome would attract on its repeats high quantities of chromatin-modifying proteins, which would in turn lead to a global modification of the chromatin state on other chromosomes, and in the end would affect the accessibility of splicing factors to the nascent transcripts.

Here, the impact of TEs on the splicing machinery would thus be indirect and not specific to particular genes. Finally, genes involved in sexual development and sexual functions seem to evolve faster than other genes [ , ].

These observations of positive selection and rapid evolution are not really consistent with earlier observations of the sex determination and differentiation cascade. A renewal of this initial proposition has been proposed by Herpin et al. Knowing that TEs are a source of genomic diversification, studying the evolution of sexual development genes in the perspective of TEs, just as the evolution of their regulation, could reveal interesting trends.

A perspective could be to investigate RNA-seq dataset for species-specific sex-biased genes associated to TE location variation between closely related species to reveal candidate genes recently controlled by TEs. Global approaches by sequencing piRNAs and mapping them to sex-biased genes could also give more clues about the regulation and evolution of genes involved in sexual development and function. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.

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