Internuclear gene silencing in Phytophthora infestans.

نویسندگان

  • P van West
  • S Kamoun
  • J W van 't Klooster
  • F Govers
چکیده

Transformation of the diploid oomycete plant pathogen Phytophthora infestans with antisense, sense, and promoter-less constructs of the coding sequence of the elicitin gene inf1 resulted in transcriptional silencing of both the transgenes and the endogenous gene. Since heterokaryons obtained by somatic fusion of an inf1-silenced transgenic strain and a wild-type strain displayed stable gene silencing, inf1 silencing is dominant and acts in trans. Inf1 remained silenced in nontransgenic homokaryotic progeny from the silenced heterokaryons, thereby demonstrating that the presence of transgenes is not essential for maintaining the silenced status of the endogenous inf1 gene. These findings support a model reminiscent of paramutation and involving a trans-acting factor that is capable of transferring a silencing signal between nuclei.

برای دانلود 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

Internuclear gene silencing in Phytophthora infestans is established through chromatin remodelling.

In the plant pathogen Phytophthora infestans, nuclear integration of inf1 transgenic DNA sequences results in internuclear gene silencing of inf1. Although silencing is regulated at the transcriptional level, it also affects transcription from other nuclei within heterokaryotic cells of the mycelium. Here we report experiments exploring the mechanism of internuclear gene silencing in P. infesta...

متن کامل

Can silencing of transposons contribute to variation in effector gene expression in Phytophthora infestans?

Transposable elements are ubiquitous residents in eukaryotic genomes. Often considered to be genomic parasites, they can lead to dramatic changes in genome organization, gene expression, and gene evolution. The oomycete plant pathogen Phytophthora infestans has evolved a genome organization where core biology genes are predominantly located in genome regions that have relatively few resident tr...

متن کامل

Plant-mediated gene silencing restricts growth of the potato late blight pathogen Phytophthora infestans

Phytophthora infestans is an oomycete that causes severe damage to potato, and is well known for its ability to evolve rapidly in order to overcome resistant potato varieties. An RNA silencing strategy was evaluated here to clarify if small interfering RNA homologous to selected genes in P. infestans could be targeted from the plant host to reduce the magnitude of the infection. As a proof-of-c...

متن کامل

U-box E3 ubiquitin ligase PUB17 acts in the nucleus to promote specific immune pathways triggered by Phytophthora infestans

Ubiquitination regulates many processes in plants, including immunity. The E3 ubiquitin ligase PUB17 is a positive regulator of programmed cell death (PCD) triggered by resistance proteins CF4/9 in tomato. Its role in immunity to the potato late blight pathogen, Phytophthora infestans, was investigated here. Silencing StPUB17 in potato by RNAi and NbPUB17 in Nicotiana benthamiana by virus-induc...

متن کامل

Comparisons of Ribosomal Protein Gene Promoters Indicate Superiority of Heterologous Regulatory Sequences for Expressing Transgenes in Phytophthora infestans.

Molecular genetics approaches in Phytophthora research can be hampered by the limited number of known constitutive promoters for expressing transgenes and the instability of transgene activity. We have therefore characterized genes encoding the cytoplasmic ribosomal proteins of Phytophthora and studied their suitability for expressing transgenes in P. infestans. Phytophthora spp. encode a stand...

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

برای دانلود 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

عنوان ژورنال:
  • Molecular cell

دوره 3 3  شماره 

صفحات  -

تاریخ انتشار 1999