Mutations in ccf, a novel Drosophila gene encoding a chromosomal factor, affect progression through mitosis and interact with Pc-G mutations.

نویسندگان

  • L Kodjabachian
  • M Delaage
  • C Maurel
  • R Miassod
  • B Jacq
  • R Rosset
چکیده

We report herein the isolation of ccf, a new gene located in region 82E and essential for Drosophila development. This gene, expressed throughout development, encodes a novel product of 68 kDa which is found in the nucleus during interphase and labels, in a novel pattern, centrosomes and chromosome arms during mitosis. Mutations in ccf give rise to late larvae with small imaginal discs and to adults showing appendages of reduced size, consistent with CCF involvement in cell proliferation. Neuroblast squash analyses show that CCF is required for proper condensation of mitotic chromosomes and, therefore, for progression through mitosis. Furthermore, we observe that adult ccf mutants as well as animals overexpressing CCF during larval stages exhibit homeotic transformations. We also find that mutations in the Pc-G genes Polycomb, polyhomeotic and Enhancer of zeste are enhanced by ccf mutations. Finally, we show that the CCF protein binds to specific sites on polytene chromosomes, many of which are shared with the Posterior sex combs Pc-G protein. Together, these results suggest a role for the CCF protein in the maintenance of chromosome structure during mitosis and interphase.

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

جهش جدید هموپلاسمیک T4216C میتوکندریایی در افراد ایرانی مبتلا به بیماری فردریش اتاکسیا

Introduction: The mitochondrial defects in Friedreich ataxia (FRDA) have been reported in many researches. Friedreich ataxia is an autosomal recessive neurodegenerative disorder caused by decreased expression of the Frataxin protein. Frataxin deficiency leads to excessive free radical production and dysfunction of respiratory chain complexes. Mitochondrial DNA (mtDNA) could be considered as a c...

متن کامل

Molecular and Clinical Characterization of 7 Iranian Patients with Severe Congenital Factor V Deficiency: Identification of 4 Novel Mutations

Background and Aims: Congenital factor V (FV) deficiency is a rare bleeding disorder with 1 in 1000000 persons in the general population. Individuals with FV activity <1% and very low FV antigen levels are characterized as severe FV deficient patients. Little data is available about the molecular basis of this bleeding disorder in Iran. Materials and Methods: We analyzed 7 unrelated Iranian FV...

متن کامل

Molecular Characterization of the Factor IX Gene in 28 Iranian Hemophilia B Patients

Background: Heterogeneous mutations in the human coagulation factor IX gene lead to an X-linked recessive bleeding disorder known as hemophilia B. The disease is distributed worldwide with no ethnic or geographical priority. Materials and Methods: The aim of this study was to characterize the factor IX gene mutations in 28 unrelated Iranian hemophilia B patients. Polymerase chain reaction (PCR)...

متن کامل

Novel mutations in ATP7B gene of Wilson\'s disease in Iranian patients

Bacground: Wilson's disease is a rare autosomal recessive disorder characterized by toxic accumulation of copper in liver and brain. The disorder is caused by mutations in the ATP7B gene, encoding a copper transporting P-type ATPase. Characterization of the spectrum of mutations in this gene is important both for diagnosis and genetic counseling of the families. Materials and Methods: We enrol...

متن کامل

Novel Missense Mitochondrial ND4L Gene Mutations in Friedreich's Ataxia

Objective(s) The mitochondrial defects in Friedreich's ataxia have been reported in many researches. Mitochondrial DNA is one of the candidates for defects in mitochondrion, and complex I is the first and one of the largest catalytic complexes of oxidative phosphorylation (OXPHOS) system. Materials and Methods We searched the mitochondrial ND4L gene for mutations by TTGE and sequencing on 30...

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:
  • The EMBO journal

دوره 17 4  شماره 

صفحات  -

تاریخ انتشار 1998