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

Lim, Young-Mi; Hayashi, Shigeo; Tsuda, Leo

doi:10.1371/journal.pone.0037028

Cited by 11 publications

(22 citation statements)

References 42 publications

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“…, ; Lim et al . ). Therefore, we explored the possibility that the corepressor function of Ebi is involved in cyclin‐dependent transcriptional regulation.…”

Section: Resultsmentioning

confidence: 97%

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Ebi alleviates excessive growth signaling through multiple epigenetic functions in Drosophila

2013

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As multicellular organisms develop, many cells permanently stop dividing and undergo terminal differentiation. The G1 phase of the cell cycle is thought to be the critical decision point for differentiation. Many growth factors, such as epidermal growth factor, are involved in regulating the G1 to S phase transition, and aberrant activation of growth factor signaling is one of the critical causes of tumor formation. Therefore, each cell must have proper mechanisms to suppress inappropriate/excessive activation of growth factor signaling, but the underlying molecular mechanisms remain undefined. Here, we found that ebi, a Drosophila homologue of genes encoding transducin-b-like 1 and transducin-b-like 1-related protein, mitigated excess growth stimulation by taking advantage of its distinct epigenetic functions. Ebi acted as a corepressor of transcription by forming a complex with retinoblastoma family protein (RBF), a Drosophila homologue of retinoblastoma, and regulating the expression of specific target genes of the Rbf/E2F pathway. Furthermore, ebi also sustained expression of certain genes, including Rbf, encoding factors that inhibit progression out of G1. Our genetic studies suggest that the antagonistic function of ebi against the Polycomb group silencing complex plays a role in the G1/S phase transition.

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“…, ; Lim et al . ). Therefore, we explored the possibility that the corepressor function of Ebi is involved in cyclin‐dependent transcriptional regulation.…”

Section: Resultsmentioning

confidence: 97%

“…, ; Lim et al . ). These multiple functions of ebi appear to be evolutionarily conserved, as TBL1 acts as an ubiquitin ligase as well as part of a corepressor complex (Matsuzawa & Reed, ; Perissi et al .…”

Section: Introductionmentioning

confidence: 97%

Ebi alleviates excessive growth signaling through multiple epigenetic functions in Drosophila

2013

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“…, ; Lim et al . ). These multiple functions of ebi appear to be evolutionarily conserved; TBL1 seems to have a function as an ubiquitin‐ligase, in addition to the co‐repressor complex activity (Matsuzawa & Reed ; Perissi et al .…”

Section: Introductionmentioning

confidence: 97%

“…Recent study suggests that the co‐repressor activity in the sensory cells survival might be evolutionarily conserved; ebi mutation caused age‐dependent retinal degeneration phenotype in Drosophila (Lim et al . ). Introducing a similar mutation of TBL1 observed in OASD patient into Ebi (C‐terminal truncation) caused age‐dependent retinal degeneration, and Ebi cDNA completely rescued the phenotype.…”

Section: Introductionmentioning

confidence: 97%

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Regulatory system for the G1‐arrest during neuronal development in Drosophila

Tsuda

Lim

2014

Dev Growth Differ

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Neuronal network consists of many types of neuron and glial cells. This diversity is guaranteed by the constant cell proliferation of neuronal stem cells following stop cell cycle re-entry, which leads to differentiation during development. Neuronal differentiation occurs mainly at the specific cell cycle phase, the G1 phase. Therefore, cell cycle exit at the G1 phase is quite an important issue in understanding the process of neuronal cell development. Recent studies have revealed that aberrant S phase re-entry from the G1 phase often links cellular survival. In this review we discuss the different types of G1 arrest on the process of neuronal development in Drosophila. We also describe the issue that aberrant S phase entry often causes apoptosis, and the same mechanism might contribute to sensory organ defects, such as deafness.

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Ocular albinism with infertility and late‐onset sensorineural hearing loss

Fabian‐Jessing

Vestergaard

Plomp

et al. 2018

American J of Med Genetics Pt A

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Ocular albinism type 1 (OA1) is caused by mutations in the GPR143 gene located at Xp22.2. The manifestations, which are due to hypopigmentation, are confined to the eyes and optic pathway. OA1 associated with late-onset sensorineural hearing loss was previously reported in a single family and hypothesized to be caused by a contiguous gene deletion syndrome involving GPR143 and the adjacent gene, TBL1X. Here, we report on a family with OA1, infertility, late-onset sensorineural hearing loss, and a small interstitial Xp microdeletion including the GPR143, TBL1X, and SHROOM2 genes. In addition, we re-examined a patient previously described with OA1, infertility and a similar Xp deletion with audiologic follow-up showing a late-onset sensorineural hearing loss. Our results raise an intriguing question about the possibility for TBL1X (absence) involvement in this type of hearing loss. However, our study cannot claim a causative relationship and more convincing evidence is needed before the hypothesis can be accepted that TBL1X could be involved in late-onset sensorineural hearing loss and that ocular albinism with late-onset sensorineural hearing loss can present itself as a contiguous gene deletion/microdeletion syndrome. The finding of infertility in all affected male patients demonstrates that this deletion, including the SHROOM2 gene, may be a potentially causative X-linked genetic factor of male infertility.

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

Cited by 11 publications

References 42 publications

Ebi alleviates excessive growth signaling through multiple epigenetic functions in Drosophila

Ebi alleviates excessive growth signaling through multiple epigenetic functions in Drosophila

Regulatory system for the G1‐arrest during neuronal development in Drosophila

Ocular albinism with infertility and late‐onset sensorineural hearing loss

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