ATAD3 gene cluster deletions cause cerebellar dysfunction associated with altered mitochondrial DNA and cholesterol metabolism

نویسندگان

  • Radha Desai
  • Ann E. Frazier
  • Romina Durigon
  • Harshil Patel
  • Aleck W. Jones
  • Ilaria Dalla Rosa
  • Nicole J. Lake
  • Alison G. Compton
  • Hayley S. Mountford
  • Elena J. Tucker
  • Alice L. R. Mitchell
  • Deborah Jackson
  • Abdul Sesay
  • Miriam Di Re
  • Lambert P. van den Heuvel
  • Derek Burke
  • David Francis
  • Sebastian Lunke
  • George McGillivray
  • Simone Mandelstam
  • Fanny Mochel
  • Boris Keren
  • Claude Jardel
  • Anne M. Turner
  • P. Ian Andrews
  • Jan Smeitink
  • Johannes N. Spelbrink
  • Simon J. Heales
  • Masakazu Kohda
  • Akira Ohtake
  • Kei Murayama
  • Yasushi Okazaki
  • Anne Lombès
  • Ian J. Holt
  • David R. Thorburn
  • Antonella Spinazzola
چکیده

Although mitochondrial disorders are clinically heterogeneous, they frequently involve the central nervous system and are among the most common neurogenetic disorders. Identifying the causal genes has benefited enormously from advances in high-throughput sequencing technologies; however, once the defect is known, researchers face the challenge of deciphering the underlying disease mechanism. Here we characterize large biallelic deletions in the region encoding the ATAD3C, ATAD3B and ATAD3A genes. Although high homology complicates genomic analysis of the ATAD3 defects, they can be identified by targeted analysis of standard single nucleotide polymorphism array and whole exome sequencing data. We report deletions that generate chimeric ATAD3B/ATAD3A fusion genes in individuals from four unrelated families with fatal congenital pontocerebellar hypoplasia, whereas a case with genomic rearrangements affecting the ATAD3C/ATAD3B genes on one allele and ATAD3B/ATAD3A genes on the other displays later-onset encephalopathy with cerebellar atrophy, ataxia and dystonia. Fibroblasts from affected individuals display mitochondrial DNA abnormalities, associated with multiple indicators of altered cholesterol metabolism. Moreover, drug-induced perturbations of cholesterol homeostasis cause mitochondrial DNA disorganization in control cells, while mitochondrial DNA aggregation in the genetic cholesterol trafficking disorder Niemann-Pick type C disease further corroborates the interdependence of mitochondrial DNA organization and cholesterol. These data demonstrate the integration of mitochondria in cellular cholesterol homeostasis, in which ATAD3 plays a critical role. The dual problem of perturbed cholesterol metabolism and mitochondrial dysfunction could be widespread in neurological and neurodegenerative diseases.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Role of Mitochondria in Ataxia-Telangiectasia: Investigation of Mitochondrial Deletions and Haplogroups

Ataxia-Telangiectasia (AT) is a rare human neurodegenerative autosomal recessive multisystem disease that is characterized by a wide range of features including, progressive cerebellar ataxia with onset during infancy, occulocutaneous telangiectasia, susceptibility to neoplasia, occulomotor disturbances, chromosomal instability and growth and developmental abnormalities. Mitochondrial DNA (mtDN...

متن کامل

Human Mitochondrial DNA-Protein Complexes Attach to a Cholesterol-Rich Membrane Structure

The helicase Twinkle is indispensable for mtDNA replication in nucleoids. Previously, we showed that Twinkle is tightly membrane-associated even in the absence of mtDNA, which suggests that Twinkle is part of a membrane-attached replication platform. Here we show that this platform is a cholesterol-rich membrane structure. We fractionated mitochondrial membrane preparations on flotation gradien...

متن کامل

Mitochondrial nucleoid interacting proteins support mitochondrial protein synthesis

Mitochondrial ribosomes and translation factors co-purify with mitochondrial nucleoids of human cells, based on affinity protein purification of tagged mitochondrial DNA binding proteins. Among the most frequently identified proteins were ATAD3 and prohibitin, which have been identified previously as nucleoid components, using a variety of methods. Both proteins are demonstrated to be required ...

متن کامل

The AAA+ protein ATAD3 has displacement loop binding properties and is involved in mitochondrial nucleoid organization

Many copies of mammalian mitochondrial DNA contain a short triple-stranded region, or displacement loop (D-loop), in the major noncoding region. In the 35 years since their discovery, no function has been assigned to mitochondrial D-loops. We purified mitochondrial nucleoprotein complexes from rat liver and identified a previously uncharacterized protein, ATAD3p. Localization studies suggested ...

متن کامل

Mitochondrial Genetic Variation in Iranian Infertile Men with Varicocele

Objective Several recent studies have shown that mitochondrial DNA mutations lead to major disabilities and premature death in carriers. More than 150 mutations in human mitochondrial DNA (mtDNA) genes have been associated with a wide spectrum of disorders. Varicocele, one of the causes of infertility in men wherein abnormal inflexion and distension of veins of the pampiniform plexus is observe...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 140  شماره 

صفحات  -

تاریخ انتشار 2017