Hubbry Logo
Y linkageY linkageMain
Open search
Y linkage
Community hub
Y linkage
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Y linkage
Y linkage
Y linkage
View on Wikipedia
from Wikipedia
Y-linked inheritance
Pedigree tree showing the inheritance of a Y-linked trait

Y linkage, also known as holandric inheritance (from Ancient Greek ὅλος hólos, "whole" + ἀνδρός andrós, "male"),[1] describes traits that are produced by genes located on the Y chromosome. It is a form of sex linkage.

Y linkage can be difficult to detect. This is partly because the Y chromosome is small and contains fewer genes than the autosomal chromosomes or the X chromosome. It is estimated to contain about 200 genes. It was once believed that the human Y chromosome was thought to have little importance.[2] While the Y-chromosome is sex-determining in humans and some other species, not all genes that play a role in sex determination are Y-linked. The Y-chromosome, generally does not undergo genetic recombination except at small pseudoautosomal regions. The majority of the Y-chromosome genes that do not recombine are located in the "non-recombining region".[3]

For a trait to be considered Y linkage, it must exhibit the following characteristics:

  • occurs only in males
  • appears in all sons of males who exhibit that trait
  • is absent from daughters of trait carriers; instead the daughters are phenotypically normal and do not have affected offspring.[4]

These requirements were established by the pioneer of Y linkage, Curt Stern. Stern detailed in his paper genes he suspected to be Y-linked.[4] His requirements at first made Y linkage hard to prove. In the 1950s using human pedigrees, many genes were incorrectly determined to be Y-linked.[5] Later research adopted more advanced techniques and more sophisticated statistical analysis.[6] Hairy ears are an example of a gene once thought to be Y-linked in humans; however, that hypothesis was discredited.[5] Due to advancements in DNA sequencing, Y linkage is getting easier to determine and prove. The Y-chromosome has been entirely mapped,[7] revealing many Y-linked traits.[8]

Y linkage is similar to, but different from X linkage; although, both are forms of sex linkage. X linkage can be genetically linked and sex-linked, while Y linkage can only be genetically linked. This is because males' cells have only one copy of the Y-chromosome. X-chromosomes have two copies, one from each parent permitting recombination. The X chromosome contains more genes and is substantially larger.

Some ostensibly Y-linked traits have not been confirmed. One example is hearing impairment. Hearing impairment was tracked in one specific family and through seven generations all males were affected by this trait. However, this trait occurs rarely and has not been entirely resolved.[9]

Y-chromosome deletions are a frequent genetic cause of male infertility.

Y-linkage in non-human animals

[edit]

Guppies

[edit]

In guppies, Y-linked genes help determine sex selection. This is done indirectly by traits that allow the guppy to appear more attractive to a prospective mate. These traits were shown to be on the Y-chromosome and thus Y-linked.[10] Also in guppies, it appears that the four measures of sexual activity is Y-linked.[11]

Rats

[edit]

Hypertension, or high blood pressure, appears to be Y-linked in the hypertensive rat. One locus was autosomal. However, the second component appeared to be Y-linked. This held through the third generation of rats. Male offspring with a hypertensive father had significantly higher blood pressure than male offspring with a hypertensive mother indicating that a component of the trait was Y-linked. The results were not the same in females as in males, further hinting at a Y-component.[12]

Genes on the human Y chromosome

[edit]

In general, traits that exist on the Y chromosome are Y-linked because they only occur on that chromosome and do not change in recombination.

As of 2000, a number of genes were known to be Y-linked, including:[13]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Y linkage

View on Grokipedia
from Grokipedia
Y linkage, also known as holandric inheritance, is a pattern of genetic in which a variant is located on the and is transmitted exclusively from father to son, affecting only biological males since females lack a . The human is one of the two sex chromosomes, spanning approximately 62 million base pairs and containing 106 protein-coding genes that primarily encode proteins involved in male-specific functions such as sex determination and . Unlike autosomes or the , the male-specific region of the (MSY) does not undergo recombination during , resulting in complete linkage of genes within this region and their as a single unit across male generations. This non-recombining nature contributes to the evolutionary degeneration of the , which has lost many genes over time compared to its ancestral homolog. Confirmed Y-linked traits in humans are rare due to the limited gene content of the , but notable examples include Y chromosome infertility, caused by deletions in the azoospermia factor (AZF) regions that disrupt genes essential for sperm production, leading to or severe in affected males. Another example is certain cases of Swyer syndrome, a form of 46,XY gonadal dysgenesis, resulting from variants in the SRY gene on the that prevent the initiation of male gonadal development, causing individuals with a Y chromosome to develop external genitalia. These conditions illustrate the 's critical role in male , with affected males unable to pass the trait to daughters but transmitting it to all sons.

Basics of Sex Chromosome Inheritance

Structure and Role of X and Y Chromosomes

In mammals, sex is determined by a dimorphic pair of : the larger and the smaller . The human spans approximately 155 megabases (Mb) and contains around 800–900 protein-coding genes, contributing to a wide array of functions including dosage compensation via in females. In contrast, the is much smaller at about 59 Mb, with its male-specific region (MSY) comprising roughly 23 Mb of that harbors approximately 106 protein-coding genes, most of which are involved in male-specific processes such as . Recent complete sequencing of the (T2T-CHM13 assembly, 2023) has resolved previous gaps, confirming this updated gene count and a total Y length of about 62 Mb. This size disparity reflects the evolutionary divergence of the , where the Y has undergone significant degeneration and loss of genetic material compared to the X. The XY system in mammals establishes male heterogamety, where males possess one X and one Y chromosome (XY), while females have two X chromosomes (XX). This heterogametic configuration in males leads to the inheritance of the Y chromosome exclusively from fathers to sons, underpinning the patrilineal transmission central to Y linkage. Recombination between the X and Y chromosomes is restricted but occurs in specific pseudoautosomal regions (PARs), which flank the MSY and facilitate obligatory pairing during male meiosis. The short arm PAR1 spans about 2.7 Mb, and the long arm PAR2 covers approximately 0.33 Mb; genes within these regions escape Y-specific degeneration due to X-Y exchange. Outside the PARs, the non-recombining MSY evolves independently, accumulating male-specific sequences without crossover with the X. The primary role of the in male sex determination stems from the SRY gene located on its short arm, which acts as the testis-determining factor by initiating gonadal differentiation toward testes during embryonic development. Without SRY, the default developmental pathway leads to ovarian formation, highlighting the Y's critical, albeit limited, functional contribution beyond the PARs. This mechanism ensures the stability of the XY system across mammalian .

Holandric Inheritance Pattern

Holandric inheritance, also known as Y-linked , refers to the pattern of transmission for traits encoded exclusively by genes on the , which is present only in males. These traits are passed directly from an affected father to all of his sons, while daughters receive no Y chromosome and thus cannot inherit or express the trait. This mode of inheritance results in phenotypic expression limited to males across generations, with no skipping of generations in the male line. In pedigree analysis, holandric inheritance exhibits a distinctive pattern where only males are affected, and the trait appears in every generation through father-to-son transmission exclusively. Affected individuals are always male, all sons of an affected father inherit the trait, and no female-to-male or female transmission occurs, creating a vertical lineage confined to males. This contrasts sharply with X-linked inheritance, where traits on the show no father-to-son transmission because sons inherit their single X chromosome from their mother, not their father, leading to potential skipping in male lines and expression in carrier females. Theoretical pedigrees illustrate this pattern clearly. For example, in a three-generation :
  • Generation I: An affected (Y-linked trait present) mates with an unaffected , producing two sons (both affected) and two daughters (both unaffected).
  • Generation II: Each affected son mates with an unaffected , yielding four grandsons (all affected) and four granddaughters (all unaffected).
  • Generation III: The affected grandsons continue the pattern, transmitting the trait only to their sons.
This unbroken male-specific transmission distinguishes holandric inheritance from other modes.

Y Linkage in Humans

Human Y Chromosome Composition

The human Y chromosome is an acrocentric structure characterized by a short p-arm, a long q-arm, a centromere, and extensive heterochromatic regions, particularly in the distal portion of the q-arm known as Yq12. The p-arm primarily encompasses the pseudoautosomal region 1 (PAR1), which facilitates recombination with the X chromosome, while the q-arm houses the majority of the male-specific region (MSY) and the smaller pseudoautosomal region 2 (PAR2). The centromere, located near the junction of the arms, consists of repetitive alpha-satellite DNA that ensures proper segregation during cell division. Heterochromatic segments, comprising satellite repeats such as DYZ1 and DYZ2 arrays, contribute significantly to length variation among individuals, with Yq12 alone accounting for up to 30-40 megabases of highly repetitive, gene-poor DNA. Sequencing of the human began with the first draft assembly in 2003, which covered about 95% of the euchromatic portion of the MSY and identified key structural features despite challenges from repetitive sequences. Subsequent refinements addressed gaps in palindromic and heterochromatic areas, culminating in the telomere-to-telomere (T2T) assembly in 2023, which provided the complete 62,460,029 sequence of the HG002 . This latest assembly resolved over 30 million previously unsequenced bases, including the full heterochromatic Yq12, and annotated a total of 106 protein-coding genes across the chromosome. The non-recombining MSY, which constitutes approximately 95% of the Y chromosome's length, is subdivided into distinct regions: the X-degenerate region featuring single-copy genes with homologs on the , the ampliconic region with multi-copy gene families embedded in large palindromic repeats, and minor X-transposed segments derived from ancient X-Y translocations. In contrast, the recombining PAR regions—PAR1 (~2.7 Mb on the p-arm) and PAR2 (~0.33 Mb on the q-arm)—contain genes that escape Y-specific degeneration due to obligatory pairing with the . These divisions reflect the Y's evolutionary history, with the MSY's isolation promoting sequence divergence from the . Overall gene density on the is low, at about 1.1 s per megabase, compared to the average, reflecting its gene-poor nature outside male-specific functions. However, the ampliconic region exhibits higher density due to via eight large palindromes (P1-P8), which span roughly 5.5 megabases and enable arm-to-arm gene conversion to mitigate degenerative mutations. These palindromic structures, with arms sharing over 99.9% identity, host multi-copy s such as those in the DAZ and RBMY families, amplifying expression critical for without increasing overall size excessively.

Key Y-Linked Genes and Associated Traits

The SRY (sex-determining region Y) gene, located at Yp11.2 on the short arm of the human , encodes a critical for determination by initiating testis development in the bipotential during embryogenesis. Mutations in SRY, often in the high-mobility group DNA-binding domain, disrupt this process and account for approximately 10-15% of cases of 46, (Swyer syndrome), leading to female external genitalia despite a 46,XY . The TSPY (testis-specific protein Y-encoded) consists of multiple copies (typically 23-64 per ) clustered in a 434 kb amplicon on Yp11.32, where the encoded proteins promote spermatogonial proliferation and early . Copy number variations in TSPY, with fewer than 21 or more than 55 copies, are associated with reduced yield and increased risk of , as observed in studies of across diverse Y lineages. Several other Y-linked genes contribute to male-specific functions. The AMELY (amelogenin Y-linked) gene on Yp11.2 produces a minor isoform of protein, which supports during formation, though its role is secondary to the X-linked counterpart and not essential for enamel development. The UTY (ubiquitously transcribed tetratricopeptide repeat containing, Y-linked) on Yq11 functions as a H3K27 demethylase, regulating in processes such as spermatogonial proliferation and immune modulation; its deficiency impairs male fertility and increases susceptibility to conditions like . The DAZ (deleted in azoospermia) family, comprising four copies in the AZFc region on Yq11, encodes RNA-binding proteins essential for maturation and production; deletions affecting DAZ occur in 10-15% of azoospermic or severely oligozoospermic men, causing spermatogenic . These genes underpin key male traits, including testis determination and , with disruptions primarily manifesting as rather than overt physical phenotypes. No common visible phenotypic traits (e.g., height, hair patterns, eye color) are strictly Y-linked; older examples like hairy ears or webbed toes are unconfirmed by modern genomics. In forensics, Y-chromosomal short (Y-) markers and haplogroups in the non-recombining portion of the enable paternal lineage tracing and male-specific identification in mixed DNA samples, aiding paternity testing, population genetics studies, and criminal investigations without establishing direct paternity.

Y Linkage in Non-Human Animals

Y Linkage in Fish: Guppy Examples

The (Poecilia reticulata) serves as a prominent for studying Y linkage in non-mammalian vertebrates, featuring an where the harbors genes for male-specific ornamental traits. These traits, primarily expressed in males due to Y-linked inheritance, exemplify holandric transmission from fathers to sons, bypassing recombination in the male-specific Y (MSY) region. The in guppies is largely homomorphic with the X but includes a non-recombining MSY segment on linkage group 12, spanning approximately 5 Mbp as of recent 2025 analyses, which suppresses crossing over and preserves male-advantageous alleles. Prominent Y-linked traits in guppies include the orange spot (OS) coloration and black caudal peduncle (BCP) spots, both of which contribute to male sexual attractiveness. The OS trait, characterized by carotenoid-based orange pigmentation on the body and fins, shows sex-linked , with quantitative genetic analyses revealing strong paternal transmission and additive variance primarily attributable to Y-chromosomal loci. Similarly, the BCP trait manifests as a dominant black marking at the base of the tail, controlled by the sex-linked Bcp gene located on both X and Y chromosomes, which maps approximately 5.1 map units from the sex-determining region (SdR) and can be expressed in females when homozygous on the X. These traits exhibit extreme polymorphism across populations, enhancing male mating success through female preferences. Genetic mapping efforts have the sex-determining region on linkage group 12, with a recent 2025 study mapping a male-specific region of ~5 Mbp at the distal end of the . Earlier work candidate genes like GADD45G-like isoforms in a minimal interval for sex determination. No recombination occurs within the MSY, ensuring tight linkage between the SdR and associated genes, as evidenced by recombination frequencies in controlled crosses. This genetic architecture facilitates the accumulation of sexually selected variants without dilution from X-chromosomal recombination. From an evolutionary perspective, sexual selection imposed by female has driven the diversification of Y-linked ornamentation in guppies, with studies from the 1980s onward highlighting how predation gradients and preference strength select for conspicuous colors like OS and BCP. Seminal work by John Endler in the 1980s demonstrated natural and sexual selection on color patterns in wild Trinidadian populations, while 1990s-2000s quantitative genetic analyses confirmed Y-linkage as a mechanism resolving intralocus by confining attractive but costly traits to males. This pattern underscores the role of the in rapid adaptive evolution of poeciliid mating systems.

Y Linkage in Mammals: Rat Examples

The in the ( norvegicus) shares structural and functional similarities with its counterpart, including a -poor composition dominated by male-specific regions involved in sex determination and , though it features species-specific variations such as multiple copies of the Sry gene—unlike the single copy in humans and mice. These duplications, with up to 11 loci and nine distinct variants identified in some strains like SHR, contribute to testicular development but may also influence quantitative traits like susceptibility. Y-linked traits in rats prominently include behavioral phenotypes such as increased and territoriality, particularly in the spontaneously hypertensive rat (SHR) strain, where the SHR-derived elevates serum testosterone levels and reduces serotonin content, leading to heightened intermale in resident-intruder tests and intra-colony interactions. This father-to-son transmission pattern was first evidenced in early consomic strain studies during the , demonstrating strict holandric of aggressive behaviors independent of autosomal or X-linked factors. Additionally, the Y chromosome harbors genes critical for , including Sry for gonadal differentiation and Eif2s3y for spermatogonial proliferation; variants in these loci underlie differences across strains. Research on rat Y linkage advanced significantly in the 1990s through quantitative trait locus (QTL) mapping in consomic and recombinant inbred strains, identifying Y-chromosomal contributions to regulation—such as a locus elevating in SHR males—and outcomes, including production efficiency. These studies highlighted the Y chromosome's role in integrating physiological and behavioral traits, providing a mammalian model contrasting Y-linked conditions by emphasizing polygenic interactions in .

Evolutionary and Clinical Perspectives

Evolution and Degeneration of the Y Chromosome

The in mammals originated approximately 180 million years ago from a homologous pair of autosomes, when a region containing the sex-determining SRY differentiated, with SRY itself arising from a duplication and modification of the X-linked SOX3 . This event marked the beginning of sex chromosome evolution, where the proto-Y acquired male-determining functions, leading to the suppression of recombination with the proto-X to prevent the spread of the male-specific region to females. The degeneration of the Y chromosome began shortly after recombination suppression, as the lack of genetic exchange with the X prevented the purging of deleterious mutations, resulting in extensive gene loss over evolutionary time. Under —a process where the chromosome accumulates harmful mutations irreversibly due to its haploid, non-recombining —the Y has lost the vast majority of its original gene content, shrinking from an estimated 1,000–1,400 ancestral genes (comparable to the modern ) to roughly 70 functional protein-coding genes in humans today. This decay is exacerbated by background selection and genetic , where neutral or beneficial mutations are lost alongside deleterious ones, further eroding functional sequences. Comparative studies across species highlight varying trajectories of Y chromosome evolution: while mammalian Y chromosomes, including the one, exhibit pronounced degradation due to prolonged non-recombination, some lineages maintain more stable Y chromosomes with higher retention, often because their are evolutionarily younger or retain limited recombination opportunities. In mammals, projections based on historical loss rates suggest the Y could continue shedding genes at a pace of about one every 5–10 million years, potentially leading to further functional erosion unless offset by other mechanisms. Recent findings from the , including the first complete sequencing of the human , indicate that degeneration is not unidirectional, with evidence of gene acquisition from autosomes countering decay through duplication and amplification events. For instance, palindromic repeats on the Y facilitate the copying of essential genes, such as those involved in , while studies in and humans have documented the integration of novel autosomal sequences onto the Y, enhancing its resilience over the past 25 million years. These processes suggest a dynamic equilibrium, where gains may stabilize the Y against total loss.

Clinical Implications and Disorders

Y-chromosome microdeletions within the azoospermia factor (AZF) regions represent a primary genetic cause of , particularly non-obstructive and severe oligozoospermia, accounting for 1-10% of such cases in affected populations. These deletions occur on the long arm of the and disrupt by eliminating key genes involved in development. The three major AZF subregions—AZFa, AZFb, and AZFc—exhibit varying frequencies and phenotypic impacts, with AZFc deletions being the most prevalent at 70-80% of cases, often leading to variable sperm production that may allow for assisted in some instances. AZFa deletions, rarer at 0.5-9%, typically cause complete germ cell aplasia (), while AZFb deletions (1-7%) result in spermatogenic arrest at the stage, rendering natural impossible. Disorders of sex development linked to Y chromosome anomalies further highlight the clinical stakes of Y linkage. Swyer syndrome, or 46,XY complete , arises from mutations in the SRY gene, which fails to initiate testis formation, resulting in female external genitalia, streak gonads, and an elevated risk of gonadoblastoma despite a 46,XY . These mutations are often de novo and sporadic, with affected individuals requiring lifelong and prophylactic gonadectomy to prevent . Conversely, 46,XX testicular disorder of sex development occurs when the SRY gene translocates to an during paternal , leading to a with and small testes in approximately 1 in 20,000 males. Nearly all such cases are SRY-positive due to this translocation, though SRY-negative variants exist with more ambiguous features. Recent research as of 2024 has identified additional Y-linked contributions to disease risk in males. A study linked variants on the to an increased risk of autism spectrum disorder, providing a genetic explanation for the higher prevalence in males and illustrating holandric inheritance of susceptibility factors. Similarly, the Y-linked gene UTY has been implicated in greater susceptibility to heart failure in men, highlighting the chromosome's role beyond reproduction in cardiovascular health. Furthermore, emerging studies indicate that the Y chromosome influences immune and inflammatory responses in men, potentially contributing to sex-specific differences in disease susceptibility. These influences are not associated with simple Mendelian traits but rather complex polygenic effects, including increased risks for cancer and cardiovascular diseases linked to Y chromosome variants or loss. Screening and diagnosis for Y-linked conditions rely on a combination of cytogenetic and molecular techniques to identify anomalies early. Karyotyping provides an initial assessment of chromosomal structure, detecting large-scale Y abnormalities, while targets specific AZF regions or the SRY locus for precise microdeletion mapping. Next-generation sequencing (NGS) enhances resolution by identifying point mutations, small indels, and copy number variations across the , enabling comprehensive variant detection in infertile males or at-risk pregnancies. Prenatally, these methods—often applied following findings of —carry implications for , , and monitoring for associated risks like gonadal tumors. Therapeutic strategies for Y-linked infertility and disorders are evolving, with a focus on restoring fertility potential. For assisted reproduction, Y-haplotype matching in sperm donors—assessed via short tandem repeat (STR) profiling—helps minimize genetic overlap with the recipient's lineage, improving preimplantation genetic diagnosis accuracy and reducing risks of unintended Y-linked trait transmission in IVF cycles.

References

  1. https://medlineplus.gov/genetics/understanding/inheritance/inheritancepatterns/
  2. https://pmc.ncbi.nlm.nih.gov/articles/PMC4983133/
  3. https://medlineplus.gov/genetics/chromosome/y/
  4. https://www.nature.com/articles/s41586-023-06457-y
  5. https://pmc.ncbi.nlm.nih.gov/articles/PMC4120474/
  6. https://medlineplus.gov/genetics/condition/y-chromosome-infertility/
  7. https://medlineplus.gov/genetics/condition/swyer-syndrome/
  8. https://pmc.ncbi.nlm.nih.gov/articles/PMC2665286/
  9. https://www.ncbi.nlm.nih.gov/grc/human/data
  10. https://www.science.org/doi/10.1126/science.abj6983
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC8617835/
  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC4858793/
  13. https://pmc.ncbi.nlm.nih.gov/articles/PMC2435358/
  14. https://www.nature.com/articles/ejhg200863
  15. https://pubmed.ncbi.nlm.nih.gov/8840551/
  16. https://www.ncbi.nlm.nih.gov/books/NBK22246/
  17. https://pubmed.ncbi.nlm.nih.gov/18454134/
  18. https://bio.libretexts.org/Bookshelves/Genetics/Introduction_to_Genetics_%28Singh%29/04%253A_Pedigree_Analysis/4.03%253A_Modes_of_Inheritance
  19. https://bio.libretexts.org/Bookshelves/Genetics/Introduction_to_Genetics_%28Singh%29/10%253A_Sex_Chromosomes__Sex_Linkage/10.05%253A_Y-Linked_Genes
  20. https://learn.genetics.utah.edu/content/pigeons/sexlinkage/
  21. https://bio.libretexts.org/Courses/University_of_Arkansas_Little_Rock/Genetics_BIOL3300_%28Leacock%29/Genetics_Textbook/04%253A_Inheritance/4.04%253A_Exceptions_to_autosomal_inheritance/4.4.01%253A_Inheritance_patterns_for_X-linked_and_Y-linked_genes
  22. https://rbej.biomedcentral.com/articles/10.1186/s12958-018-0330-5
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC10752217/
  24. https://www.ncbi.nlm.nih.gov/books/NBK539886/
  25. https://pubmed.ncbi.nlm.nih.gov/39788310/
  26. https://ghr.nlm.nih.gov/condition/swyer-syndrome
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC3954084/
  28. https://www.ncbi.nlm.nih.gov/gene/7258
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC9326358/
  30. https://www.ncbi.nlm.nih.gov/gene/266
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC3247901/
  32. https://www.ncbi.nlm.nih.gov/gene/7404
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC9887415/
  34. https://www.ncbi.nlm.nih.gov/gene/1617
  35. https://pubmed.ncbi.nlm.nih.gov/7670487/
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC2702067/
  37. https://www.nature.com/articles/5201271
  38. https://pmc.ncbi.nlm.nih.gov/articles/PMC3400728/
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC5418305/
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC8457770/
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC1235289/
  42. https://academic.oup.com/g3journal/article/9/11/3867/6026816
  43. https://www.journals.uchicago.edu/doi/full/10.1086/342898
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC11960691/
  45. https://www.nature.com/articles/hdy1992120
  46. https://bioone.org/journals/zoological-science/volume-16/issue-4/zsj.16.629/Sex-Linkage-of-the-Black-Caudal-Peduncle-and-Red-Tail/10.2108/zsj.16.629.full
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC2854822/
  48. https://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-14-792
  49. https://pubmed.ncbi.nlm.nih.gov/15319574/
  50. https://www.nature.com/articles/s42003-021-02936-y
  51. https://journals.biologists.com/dev/article/137/23/3921/44191/Sry-the-master-switch-in-mammalian-sex
  52. https://www.sciencedirect.com/science/article/abs/pii/S1084952107000468
  53. https://pmc.ncbi.nlm.nih.gov/articles/PMC2567394/
  54. https://www.researchgate.net/publication/23246512_Muller%27s_Ratchet_and_the_Degeneration_of_Y_Chromosomes_A_Simulation_Study
  55. https://www.nature.com/articles/s41598-020-58997-2
  56. https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-019-0627-7
  57. https://www.sciencedirect.com/science/article/pii/S0092867406002418
  58. https://www.bbc.com/news/science-environment-17127617
  59. https://news.asu.edu/20230823-researchers-assemble-first-complete-sequence-human-y-chromosome
  60. https://www.jax.org/news-and-insights/2023/August/insights-from-fully-sequencing-43-human-y-chromosomes
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC11968182/
  62. https://arupconsult.com/ati/y-chromosome-microdeletions
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC11668820/
  64. https://tau.amegroups.org/article/view/46927/html
  65. https://rarediseases.org/rare-diseases/swyer-syndrome/
  66. https://www.ncbi.nlm.nih.gov/books/NBK1416/
  67. https://medlineplus.gov/genetics/condition/46xx-testicular-difference-of-sex-development/
  68. https://www.geisinger.org/about-geisinger/news-and-media/news-releases/2024/10/17/17/42/increased-autism-risk-linked-to-y-chromosome-geisinger-study-finds
  69. https://news.virginia.edu/content/understanding-y-chromosome-discovery-advances-fight-against-heart-failure-men
  70. https://pmc.ncbi.nlm.nih.gov/articles/PMC5643963/
  71. https://pmc.ncbi.nlm.nih.gov/articles/PMC8490013/
  72. https://jmg.bmj.com/content/61/8/727
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC5856154/
  74. https://rbej.biomedcentral.com/articles/10.1186/s12958-017-0247-4
Add your contribution
Related Hubs
User Avatar
No comments yet.