FP7Индивидуална стипендия2011–2014

MITOSKELETON · Elucidating the Roles of Proteins of Mitochondrial DNA Maintenance

7РП — „Хора“ (Действия „Мария Кюри“)

Период
2011-06-01 → 2014-07-01
Финансиране от ЕС
210 093 €
Участници
1
Схема
MC-IEF

Линиите свързват координатора с партньорите.

Накратко на български

Протеините бета-актин и немускулен миозин в митохондриите регулират поддръжката и експресията на митохондриалната ДНК. Това помага да се разбере как се постига баланс между репликацията на ДНК и производството на енергия в клетката.

Този кратък обзор е генериран от изкуствен интелект

Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.

Резултати накратко

Elucidating the Roles of Proteins of Mitochondrial DNA Maintenance

Mitochondrial DNA (mtDNA) is essential for life, as it contributes key elements of the oxidative phosphorylation system, which provides most of the cell’s energy. Although mtDNA is distinct from nuclear DNA it is wholly dependent on nuclear encoded gene products for its maintenance and expression. Mitochondrial DNA, like DNA elsewhere, is not naked but organized in nucleoprotein complexes, or nucleoids. The protein components of mitochondrial nucleoids play roles in mtDNA protection, propagation, segregation and expression. They include two elements of the actin cytoskeleton beta-actin and non-muscle myosin heavy chain IIA (NM-IIA). The beta-actin in mitochondria is located in the mitochondrial matrix, where it associates primarily with mtDNA, as a monomer or small oligomer. Targeting of an actin-interacting protein to mitochondria causes nucleoid enlargement, which may be related to persistent interaction of mitochondrial ribosomes with the mitochondrial nucleoid. Especially as, we have also found that NMIIA and NMIIB have a regulatory role in mitochondrial protein synthesis. Therefore, beta-actin and the non-muscle myosin proteins in mitochondria are predicted to contribute to achieving a balance between mtDNA replication and mitochondrial expression.

Текст от CORDIS, на английски · Данни: CORDIS, © Европейски съюз

Цел на проекта

Mitochondrial DNA defects were established as a cause of human disease over 20 years ago, and they are increasingly recognized as a contributory factor in major causes of human morbidity, such as neurodegeneration. Although mitochondrial DNA is known to be packaged with a variety of proteins, their functions are in many cases ill defined; hence this field is in its infancy. The functional characterization of DNA transacting proteins in mitochondria is critical to a full understanding of mitochondrial DNA metabolism and the human diseases that result when mitochondrial DNA is mutated. The proposed host laboratory is well recognized for high quality and innovative research in the field of mitochondrial genetics, and it has recently demonstrated that two components of the actin cytoskeleton are present inside mitochondria, where they associate with mitochondrial DNA. The planned experiments on these two proteins, will examine their role in mitochondrial DNA movement and transmission, identify protein partners and investigate a disease mouse model; collectively they aim to develop this new area of cell biology and determine the role of the ‘mitoskeleton’ in mitochondrial DNA maintenance and mitochondrial function.

Оригинален текст от CORDIS (на английски).

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Данни: CORDIS, © Европейски съюз