Disruption of FEM1C-W gene in zebra finch: evolutionary insights on avian ZW genes

Itoh, Yuichiro; Kampf, Kathy; Arnold, Arthur P.

doi:10.1007/s00412-008-0199-8

Cited by 8 publications

(8 citation statements)

References 38 publications

(40 reference statements)

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“…In the brain samples, we could confirm that this sex bias was not due to overall differences in RNA levels loaded onto the blot; the male:female ratio of GAPDH control hybridization was 1.1. A similar control measure could not be obtained for the gonads because GAPDH expression levels can differ across tissues and the results here are consistent with previous reports that the zebra finch testes express higher levels of GAPDH than ovaries [68]. …”

Section: Resultssupporting

confidence: 90%

“…This process was performed for bands hybridized with the HSD17B4 probe and the GAPDH probe. We report male:female density ratios except in the case of GADPH hybridization to the gonads, which was higher in testes than in ovaries, as in a previous report [68]. …”

Section: Methodssupporting

confidence: 82%

“…The control GAPDH hybridization indicates that the amount of male and female RNA loaded was roughly equivalent in the brain. The testicular and ovarian samples also show differential expression levels of HSD17B4, but GAPDH is likely expressed at higher levels in the testes than the ovaries, and therefore was not used as a loading control in these tissues [68]. …”

Section: Resultsmentioning

confidence: 99%

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Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4

et al. 2010

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BackgroundSteroids affect many tissues, including the brain. In the zebra finch, the estrogenic steroid estradiol (E2) is especially effective at promoting growth of the neural circuit specialized for song. In this species, only the males sing and they have a much larger and more interconnected song circuit than females. Thus, it was surprising that the gene for 17β-hydroxysteroid dehydrogenase type 4 (HSD17B4), an enzyme that converts E2 to a less potent estrogen, had been mapped to the Z sex chromosome. As a consequence, it was likely that HSD17B4 was differentially expressed in males (ZZ) and females (ZW) because dosage compensation of Z chromosome genes is incomplete in birds. If a higher abundance of HSD17B4 mRNA in males than females was translated into functional enzyme in the brain, then contrary to expectation, males could produce less E2 in their brains than females.ResultsHere, we used molecular and biochemical techniques to confirm the HSD17B4 Z chromosome location in the zebra finch and to determine that HSD17B4 mRNA and activity were detectable in the early developing and adult brain. As expected, HSD17B4 mRNA expression levels were higher in males compared to females. This provides further evidence of the incomplete Z chromosome inactivation mechanisms in birds. We detected HSD17B4 mRNA in regions that suggested a role for this enzyme in the early organization and adult function of song nuclei. We did not, however, detect significant sex differences in HSD17B4 activity levels in the adult brain.ConclusionsOur results demonstrate that the HSD17B4 gene is expressed and active in the zebra finch brain as an E2 metabolizing enzyme, but that dosage compensation of this Z-linked gene may occur via post-transcriptional mechanisms.

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Section: Resultssupporting

confidence: 90%

Section: Methodssupporting

confidence: 82%

Section: Resultsmentioning

confidence: 99%

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Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4

et al. 2010

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“…Another potential difference is in the composition of the W chromosomes. For example, zebra finches, but not chickens, have a remnant of the FEM1C (fem-1 homolog c [C. elegans] gene on the W chromosome) (Itoh et al 2009). Considering these differences, the rearrangement of the Z chromosome may have changed the architecture of the chromosome sufficiently to undermine the selection pressures favoring an MHM-mediated compensatory mechanism.…”

Section: Sex Bias and Dosage Compensation In Birdsmentioning

confidence: 99%

Sex bias and dosage compensation in the zebra finch versus chicken genomes: General and specialized patterns among birds

Itoh¹,

Replogle²,

Kim³

et al. 2010

Genome Res.

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114

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We compared global patterns of gene expression between two bird species, the chicken and zebra finch, with regard to sex bias of autosomal versus Z chromosome genes, dosage compensation, and evolution of sex bias. Both species appear to lack a Z chromosome–wide mechanism of dosage compensation, because both have a similar pattern of significantly higher expression of Z genes in males relative to females. Unlike the chicken Z chromosome, which has female-specific expression of the noncoding RNA MHM (male hypermethylated) and acetylation of histone 4 lysine 16 (H4K16) near MHM, the zebra finch Z chromosome appears to lack the MHM sequence and acetylation of H4K16. The zebra finch also does not show the reduced male-to-female (M:F) ratio of gene expression near MHM similar to that found in the chicken. Although the M:F ratios of Z chromosome gene expression are similar across tissues and ages within each species, they differ between the two species. Z genes showing the greatest species difference in M:F ratio were concentrated near the MHM region of the chicken Z chromosome. This study shows that the zebra finch differs from the chicken because it lacks a specialized region of greater dosage compensation along the Z chromosome, and shows other differences in sex bias. These patterns suggest that different avian taxa may have evolved specific compensatory mechanisms.

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“…Although the gene content of the Z chromosome is similar across bird species, the zebra finch Z chromosome shows evidence of several rearrangements relative to that of chicken (Itoh et al 2006). Other differences have also been detected in the Z chromosome of these species: (1) the existence of W chromosome repetitive sequence (ZBM)-related sequences on Z chromosome in zebra finch, but not in chicken (Itoh et al 2008); (2) the Z-linked gene, Fem1c gene, has a homologous sequence on W chromosome in zebra finch, but not in other birds (Itoh et al 2009a); and (3) the zebra finch does not have the MHM sequence and regional dosage compensation seen in chickens (Itoh et al 2007, 2010). Also, as a unique feature of zebra finch species, a germline-restricted chromosome exists only in zebra finch, not in chicken (Pigozzi and Solari 1998; Itoh et al 2009b).…”

Section: Introductionmentioning

confidence: 99%

Karyotypic polymorphism of the zebra finch Z chromosome

et al. 2011

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We describe a karyotypic polymorphism on the zebra finch Z chromosome. This polymorphism was discovered because of a difference in the position of the centromere and because it occurs at varying frequencies in domesticated colonies in the USA and Germany and among two zebra finch subspecies. Using DNA fluorescent in situ hybridization to map specific Z genes and measurements of DNA replication, we show that this polymorphism is the result of a large pericentric inversion involving the majority of the chromosome. We sequenced a likely breakpoint for the inversion and found many repetitive sequences. Around the breakpoint, there are numerous repetitive sequences and several copies of PAK3 (p21-activated kinase 3)-related sequences (PAK3Z) which showed testes-specific expression by RT-PCR. Our findings further suggest that the sequenced genome of the zebra finch may be derived from a male heterozygote for the Z chromosome polymorphism. This finding, in combination with regional differences in the frequency of the polymorphism, has important consequences for future studies using zebra finches.Electronic supplementary materialThe online version of this article (doi:10.1007/s00412-010-0308-3) contains supplementary material, which is available to authorized users.

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Disruption of FEM1C-W gene in zebra finch: evolutionary insights on avian ZW genes

Cited by 8 publications

References 38 publications

Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4

Neural expression and post-transcriptional dosage compensation of the steroid metabolic enzyme 17β-HSD type 4

Sex bias and dosage compensation in the zebra finch versus chicken genomes: General and specialized patterns among birds

Karyotypic polymorphism of the zebra finch Z chromosome

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