Targeted disruption of mouse Dach1 results in postnatal lethality

Backman, Mattias; Machoň, Ondřej; Bout, Christiaan J. van den; Krauß, Stefan

doi:10.1002/dvdy.10210

Cited by 25 publications

(22 citation statements)

References 26 publications

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“…Of the RDGN members, DAC remains perhaps the least well mechanistically understood; the fact that Dach1-null mice die postnatally with no obvious defects has provided little additional insight into its function (Table 1) (Backman et al, 2003;Davis et al, 2001a). With respect to transcription, DAC is a novel nuclear factor with the potential to promote (Ikeda et al, 2002) and to repress gene expression (Box 2) (Li et al, 2002).…”

Section: Six1/six1 Six2/six2mentioning

confidence: 99%

Signaling circuitries in development: insights from the retinal determination gene network

2005

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Section: Six1/six1 Six2/six2mentioning

confidence: 99%

Signaling circuitries in development: insights from the retinal determination gene network

2005

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“…Newborn Dach1 mutants do not show detectable abnormalities of the eye, brain, or limbs, but die within 24 hours after birth for unknown reasons (Backman et al, 2003;Davis et al, 2001a). Dach2 mutants are viable and fertile and also appear anatomically normal (Davis et al, 2006).…”

Section: Introductionmentioning

confidence: 96%

“…Knockout alleles of mouse Dach1 and Dach2 have been generated to examine the role of Dach1/2 genes during vertebrate development (Backman et al, 2003;Davis et al, 2001aDavis et al, , 2006. Newborn Dach1 mutants do not show detectable abnormalities of the eye, brain, or limbs, but die within 24 hours after birth for unknown reasons (Backman et al, 2003;Davis et al, 2001a).…”

Section: Introductionmentioning

confidence: 99%

Mouse Dach1 and Dach2 are redundantly required for Müllerian duct development

Davis

Harding

Moayedi

et al. 2008

Genesis

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dachshund/Dach gene family members encode transcriptional cofactors with highly conserved protein interaction domains and are expressed in the developing eyes, brains, and limbs in insects and vertebrates. These observations suggest that the developmental roles of dachshund/Dach in these tissues have been conserved since the divergence of arthropods and chordates. However, while Drosophila dachshund mutants have abnormalities in eye, brain, limbs, mouse Dach1 or Dach2 knockout mutants do not exhibit gross anatomical malformations in these tissues. In addition, Dach1/2 double homozygotes have intact eyes and limbs. Here we show that in Dach1/Dach2 double mutants, female reproductive tract (FRT) development is severely disrupted. This defect is associated with the Müllerian duct (MD) and not the Wolffian duct (WD), which normally differentiate into either the FRT or male reproductive tract (MRT), respectively. Dach1 and Dach2 are expressed in the MD, and in Dach1/2 double mutants, MD expression of Lim1 and Wnt7a is abnormal and MD development is disrupted. In contrast, WD and MRT development are not grossly affected. We propose that Dach1 and Dach2 proteins may redundantly control FRT formation by regulating the expression of target genes required for development of the MD. This vertebrate Dach1/2 function may have been conserved during arthropod evolution, as Drosophila dachshund mutants also exhibit an FRT phenotype.

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“…The presence of TRH throughout the central nervous system as well as in numerous peripheral organs supports a diverse range of roles for this molecule outside of the traditional HPT axis, including a potential role as a neurotransmitter. During mouse embryogenesis, Trh mRNA has been detected in the neural folds at E8.0, at the midbrain-hindbrain junction from E8.5 to E10.5, and in the developing hypothalamus from E11.5 to E18.5 (Schonemann et al, 1995;Michaud et al, 1998Michaud et al, , 2000Acampora et al, 1999;Wang and Lufkin, 2000;Keith et al, 2001;Backman et al, 2003;Goshu et al, 2004;Caqueret et al, 2006;Jukkola et al, 2006). Despite the critical role of TRH in regulating the HPT axis and its expression in developing neural structures, mice deficient in Trh are viable and fertile (Yamada et al, 1997(Yamada et al, , 2003.…”

Section: Introductionmentioning

confidence: 99%

Dynamic expression of Thyrotropin‐releasing hormone in the mouse definitive endoderm

McKnight¹,

Hou²,

Hoodless³

2007

Developmental Dynamics

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Thyrotropin-releasing hormone (TRH) is a well-characterized regulator of the hypothalamic-pituitary-thyroid endocrine axis. Here, we describe the expression of Trh during early embryonic development in the mouse. We find Trh to be highly expressed during postimplantation stages in the mouse embryo, with expression first observed in the epiblast at embryonic day (E) 6.5. During gastrulation, Trh is expressed in the newly formed definitive endoderm cells, and at embryonic day (E) 7.75, marks the entire definitive endoderm. Subsequently, Trh mRNA levels rapidly decrease such that, by E9.0, expression in the definitive endoderm is no longer detected, after which neural expression predominates. Thus, Trh is expressed dynamically and specifically in the developing mouse definitive endoderm from E7.0 to E8.5. Trh is unique among definitive endoderm markers as it transiently marks the entire definitive endoderm population and is not expressed in the extraembryonic endoderm. Trh will be a valuable tool to study definitive endoderm formation in the mouse embryo.

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Targeted disruption of mouse Dach1 results in postnatal lethality

Cited by 25 publications

References 26 publications

Signaling circuitries in development: insights from the retinal determination gene network

Signaling circuitries in development: insights from the retinal determination gene network

Mouse Dach1 and Dach2 are redundantly required for Müllerian duct development

Dynamic expression of Thyrotropin‐releasing hormone in the mouse definitive endoderm

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