Cellular Defense and Sensory Cell Survival Require Distinct Functions of ebi in Drosophila

نویسندگان

  • Young-Mi Lim
  • Yoshimasa Yagi
  • Leo Tsuda
  • Barbara Jennings
چکیده

The innate immune response and stress-induced apoptosis are well-established signaling pathways related to cellular defense. NF-κB and AP-1 are redox-sensitive transcription factors that play important roles in those pathways. Here we show that Ebi, a Drosophila homolog of the mammalian co-repressor molecule transducin β-like 1 (TBL1), variously regulates the expression of specific genes that are targets of redox-sensitive transcription factors. In response to different stimuli, Ebi activated gene expression to support the acute immune response in fat bodies, whereas Ebi repressed genes that are involved in apoptosis in photoreceptor cells. Thus, Ebi seems to act as a regulatory switch for genes that are activated or repressed in response to different external stimuli. Our results offer clear in vivo evidence that the Ebi-containing co-repressor complex acts in a distinct manner to regulate transcription that is required for modulating the output of various processes during Drosophila development.

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

Ebi, a Drosophila homologue of TBL1, regulates the balance between cellular defense responses and neuronal survival.

Transducin β-like 1 (TBL1), a transcriptional co-repressor complex, is a causative factor for late-onset hearing impairments. Transcriptional co-repressor complexes play pivotal roles in gene expression by making a complex with divergent transcription factors. However, it remained to be clarified how co-repressor complex regulates cellular survival. We herein demonstrated that ebi, a Drosophila...

متن کامل

Rab11 is required for maintenance of cell shape via βPS integrin mediated cell adhesion in Drosophila

In eukaryotes, vesicle trafficking is regulated by the small monomeric GTPases of the Rab protein family. Rab11, (a subfamily of the Ypt/Rab gene family) an evolutionarily conserved, ubiquitously expressed subfamily of small monomeric Rab GTPases, has been implicated in regulating vesicular trafficking through the recycling of endosomal compartment. In an earlier communication, we have shown th...

متن کامل

Ebi/AP-1 Suppresses Pro-Apoptotic Genes Expression and Permits Long-Term Survival of Drosophila Sensory Neurons

Sensory organs are constantly exposed to physical and chemical stresses that collectively threaten the survival of sensory neurons. Failure to protect stressed neurons leads to age-related loss of neurons and sensory dysfunction in organs in which the supply of new sensory neurons is limited, such as the human auditory system. Transducin β-like protein 1 (TBL1) is a candidate gene for ocular al...

متن کامل

نقش استرس اکسیداتیو در تکثیر بی‌رویه و مرگ سلولی

Abstract During normal cellular activities Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) are produced. In addition to beneficial functions they play a critical role in cell death and prevent apoptosis. Every cell is equipped with an extensive antioxidant defense system to combat the excessive production of active radicals. Oxidative stress occurs with destruction of cellu...

متن کامل

Drosophila Ebi mediates Snail-dependent transcriptional repression through HDAC3-induced histone deacetylation.

The Drosophila Snail protein is a transcriptional repressor that is necessary for mesoderm formation. Here, we identify the Ebi protein as an essential Snail co-repressor. In ebi mutant embryos, Snail target genes are derepressed in the presumptive mesoderm. Ebi and Snail interact both genetically and physically. We identify a Snail domain that is sufficient for Ebi binding, and which functions...

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:

دوره 10  شماره 

صفحات  -

تاریخ انتشار 2015