Polycomb-like genes are necessary for specification of dopaminergic and serotonergic neurons in Caenorhabditis elegans.

نویسندگان

  • Yong Yang
  • Yinyan Sun
  • Xin Luo
  • Yuxia Zhang
  • Yaoyao Chen
  • E Tian
  • Robyn Lints
  • Hong Zhang
چکیده

The molecular mechanisms underlying the formation of neurons with defined neurotransmitters are not well understood. In this study, we demonstrate that the PcG-like genes in Caenorhabditis elegans, sop-2 and sor-3, regulate the formation of dopaminergic and serotonergic neurons and several other neuronal properties. sor-3 encodes a novel protein containing an MBT repeat, a domain that contains histone-binding activity and is present in PcG proteins SCM and Sfmbt in other organisms. We further show that mutations in sor-3 lead to ectopic expression of Hox genes and cause homeotic transformations. Specification of certain neuronal identities by these PcG-like genes appears to involve regulation of non-Hox gene targets. Our studies revealed that the PcG-like genes are crucial for coordinately regulating the expression of discrete aspects of neuronal identities in C. elegans.

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

A Caenorhabditis elegans Zinc Finger Transcription Factor, ztf-6, Required for the Specification of a Dopamine Neuron-Producing Lineage

Invertebrate and vertebrate nervous systems generate different types of dopaminergic neurons in distinct parts of the brain. We have taken a genetic approach to understand how the four functionally related, but lineally unrelated, classes of dopaminergic neurons of the nematode Caenorhabditis elegans, located in distinct parts of its nervous system, are specified. We have identified several gen...

متن کامل

Effects of mitochondrial dynamics genes, fzo-1 and drp-1, on dopaminergic neurodegeneration induced by environmental exposure in Caenorhabditis elegans, as a model of Parkinson’s disease

Parkinson’s disease (PD) is caused by degeneration of the dopaminergic neurons; environmental toxicants are hypothesized to play a role in PD etiology. Environmental toxicants can cause mitochondrial dysfunction through mitochondrial DNA (mtDNA) damage and production of reactive oxygen species. Serial ultraviolet C (UVC) radiation causes an accumulation of mtDNA damage and 6-hydroxydopamine (6-...

متن کامل

The Polycomb group in Caenorhabditis elegans and maternal control of germline development.

Four Caenorhabditis elegans genes, mes-2, mes-3, mes-4 and mes-6, are essential for normal proliferation and viability of the germline. Mutations in these genes cause a maternal-effect sterile (i.e. mes) or grandchildless phenotype. We report that the mes-6 gene is in an unusual operon, the second example of this type of operon in C. elegans, and encodes the nematode homolog of Extra sex combs,...

متن کامل

Caenorhabditis elegans MPP+ model of Parkinson's disease for high-throughput drug screenings.

The neurotoxin MPTP and its active metabolite MPP+ cause Parkinson's disease (PD)-like symptoms in vertebrates by selectively destroying dopaminergic neurons in the substantia nigra. MPTP/MPP+ models have been established in rodents to screen for pharmacologically active compounds. In addition to being costly and time consuming, these animal models are not suitable for large scale testings usin...

متن کامل

Mutations in Caenorhabditis elegans neuroligin-like glit-1, the apoptosis pathway and the calcium chaperone crt-1 increase dopaminergic neurodegeneration after 6-OHDA treatment

The loss of dopaminergic neurons is a hallmark of Parkinson's disease, the aetiology of which is associated with increased levels of oxidative stress. We used C. elegans to screen for genes that protect dopaminergic neurons against oxidative stress and isolated glit-1 (gliotactin (Drosophila neuroligin-like) homologue). Loss of the C. elegans neuroligin-like glit-1 causes increased dopaminergic...

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:
  • Proceedings of the National Academy of Sciences of the United States of America

دوره 104 3  شماره 

صفحات  -

تاریخ انتشار 2007