Genetic analysis of attractin homologs

@article{Walker2007GeneticAO,
  title={Genetic analysis of attractin homologs},
  author={Will P Walker and Swaroop Aradhya and Che-lin Hu and Shi-liang Shen and Wei Zhang and Arezou Azarani and Xin Yun Lu and Gregory S. Barsh and Teresa M. Gunn},
  journal={genesis},
  year={2007},
  volume={45}
}
Attractin (ATRN) and Attractin‐like 1 (ATRNL1) are highly similar type I transmembrane proteins. Atrn null mutant mice have a pleiotropic phenotype including dark fur, juvenile‐onset spongiform neurodegeneration, hypomyelination, tremor, and reduced body weight and adiposity, implicating ATRN in numerous biological processes. Bioinformatic analysis indicated that Atrn and Atrnl1 arose from a common ancestral gene early in vertebrate evolution. To investigate the genetics of the ATRN system and… 

Transgenic analysis of the physiological functions of Mahogunin ring finger‐1 isoforms

The data show that different Mgrn1 isoforms are not functionally equivalent in vivo and that the presence of only isoform I or III is sufficient for normal development, pigmentation, and neuronal integrity.

Genetic and phenotypic studies of the dark‐like mutant mouse

The results suggest dal and Atrn function in the same pathway and that identification of the dal gene will provide insight into molecular mechanisms of vacuolation in multiple cell types.

Mahoganoid and Mahogany Mutations Rectify the Obesity of the Yellow Mouse by Effects on Endosomal Traffic of MC4R Protein*

It is proposed that MGRN1 and attractin are components of an evolutionarily conserved receptor trafficking pathway and that the md and mg mutations rescue the Ay phenotypes by a primarily cAMP-independent mechanism promoting trafficking of MC4R and likely MC1R away from the lysosome toward the cell surface.

The conserved MASRPF motif in the Attractin homolog, Distracted, is required for association with Drosophila E3-ligase Mgrn1

It is shown that the MASRPF motif of Drosophila Distracted, the ortholog of ATRN and Attractin-like 1, is required for association with Drosophileila Mgrn1 (dMgrn 1) in vivo.

Attractin gene deficiency contributes to testis vacuolization and sperm dysfunction in male mice

It is concluded that the age-related Atrn gene progressively loses its function and can cause testis vacuolation and impaired sperm function, which may be responsible for the impairment of male reproductive ability.

Shades of meaning: the pigment‐type switching system as a tool for discovery

The current understanding of the pigment‐type switching pathway is outlined and the opportunities that exist for exploring the molecular basis of pleiotropic phenotypes using this model system are discussed.

Mouse models for the central melanocortin system

This review focuses on mouse models with spontaneous natural mutations as well as targeted mutations that contributed to the understanding of the central melanocortin system function in the control of energy balance.

Expression of Attractin in male reproductive tract of human and mice and its correlation with male reproduction

  • D. ChengY. Ming C. Xiong
  • Biology
    Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • 2014
It was suggested that Attractin acted as a novel active substance and was involved in male reproduction in both human and BALB/c mice, but it exerted a different expression profile in different mammal species.

Expression of Attractin in male reproductive tract of human and mice and its correlation with male reproduction

It was suggested that Attractin acted as a novel active substance and was involved in male reproduction in both human and BALB/c mice, but it exerted a different expression profile in different mammal species.

Fine-scale detection of population-specific linkage disequilibrium using haplotype entropy in the human genome

The haplotype entropy method is powerful for detecting population-specific LD embedded in short regions and should contribute to further studies aiming to decipher the evolutionary histories of modern humans.

References

SHOWING 1-10 OF 32 REFERENCES

Molecular and phenotypic analysis of Attractin mutant mice.

The results confirm that the mechanism responsible for the neuropathological alteration is a loss--rather than gain--of function, indicate that abnormal body weight in Atrn mutant mice is caused by a central process leading to increased energy expenditure, and demonstrate that pigmentation is more sensitive to levels of Atrn mRNA than are nonpigmentary phenotypes.

Attractin/mahogany/zitter plays a critical role in myelination of the central nervous system.

It is concluded that the membrane Atrn has a critical role in normalMyelination in the CNS and would provide insights into the physiology of myelination as well as the etiology of myelin diseases.

The mouse mahogany locus encodes a transmembrane form of human attractin

Observations provide new insight into the regulation of energy metabolism and indicate a molecular basis for crosstalk between melanocortin-receptor signalling and immune function.

A biochemical function for attractin in agouti-induced pigmentation and obesity

It is demonstrated in transgenic, biochemical and genetic-interaction experiments that attractin is a low-affinity receptor for agouti protein, but not Agrp, in vitro and in vivo.

Secreted and membrane attractin result from alternative splicing of the human ATRN gene.

Results suggest that a genomic event unique to mammals, LINE-1 insertion, has provided an evolutionary mechanism for regulating cell interactions during an inflammatory reaction in lymphoid tissues.

Mice with Mutations in the Mahogany Gene Atrn Have Cerebral Spongiform Changes

A new mutation characterized by mahogany coat color, sprawling gait, tremors, and severe vacuolization of cerebrum, brainstem, granular layer of cerebellum and spinal cord was discovered in a stock

Structure and function of ASP, the human homolog of the mouse agouti gene.

The cloned human homolog of the mouse agouti gene is cloned from a human chromosome 20 yeast artificial chromosome known to contain S-adenosyl homocysteine hydrolase (AHCY) and suggests a function for ag outi homologs in species that do not exhibit the characteristic phenotype of banded hairs.

Characterization of a novel binding partner of the melanocortin-4 receptor: attractin-like protein.

Co-localization analyses in mice showed co-expression of ALP in cells expressing MC4-R in a number of regions known to be important in the regulation of energy homoeostasis by melanocortins, such as the paraventricular nucleus of hypothalamus and the dorsal motor nucleus of the vagus.

Ectopic expression of the agouti gene in transgenic mice causes obesity, features of type II diabetes, and yellow fur.

It is demonstrated conclusively that the ectopic agouti expression is responsible for most, if not all, of the phenotypic traits of the dominant, obese yellow mutants.