• 제목/요약/키워드: Cofilin 1 (CFL1)

검색결과 2건 처리시간 0.02초

Expression and Functional Analysis of cofilin1-like in Craniofacial Development in Zebrafish

  • Jin, Sil;Jeon, Haewon;Choe, Chong Pyo
    • 한국발생생물학회지:발생과생식
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    • 제26권1호
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    • pp.23-36
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    • 2022
  • Pharyngeal pouches, a series of outgrowths of the pharyngeal endoderm, are a key epithelial structure governing facial skeleton development in vertebrates. Pouch formation is achieved through collective cell migration and rearrangement of pouch-forming cells controlled by actin cytoskeleton dynamics. While essential transcription factors and signaling molecules have been identified in pouch formation, regulators of actin cytoskeleton dynamics have not been reported yet in any vertebrates. Cofilin1-like (Cfl1l) is a fish-specific member of the Actin-depolymerizing factor (ADF)/Cofilin family, a critical regulator of actin cytoskeleton dynamics in eukaryotic cells. Here, we report the expression and function of cfl1l in pouch development in zebrafish. We first showed that fish cfl1l might be an ortholog of vertebrate adf, based on phylogenetic analysis of vertebrate adf and cfl genes. During pouch formation, cfl1l was expressed sequentially in the developing pouches but not in the posterior cell mass in which future pouch-forming cells are present. However, pouches, as well as facial cartilages whose development is dependent upon pouch formation, were unaffected by loss-of-function mutations in cfl1l. Although it could not be completely ruled out a possibility of a genetic redundancy of Cfl1l with other Cfls, our results suggest that the cfl1l expression in the developing pouches might be dispensable for regulating actin cytoskeleton dynamics in pouch-forming cells.

Importance of Microglial Cytoskeleton and the Actin-interacting Proteins in Alzheimer's Disease

  • Choi, Go-Eun
    • 대한의생명과학회지
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    • 제26권1호
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    • pp.1-7
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    • 2020
  • Alzheimer's disease (AD) is the most common neurodegenerative disorder and is expected to become more and more widespread as life expectancy increases. New therapeutic target, as well as the identification of mechanisms responsible for pathology, is urgently needed. Recently, microglial actin cytoskeleton has been proposed as a beneficial role in axon regeneration of brain injury. This review highlights in understanding of the characteristics of microglial actin cytoskeleton and discuss the role of specific actin-interacting proteins and receptors in AD. The precise mechanisms and functional aspects of motility by microglia require further study, and the regulation of microglial actin cytoskeleton might be a potential therapeutic strategy for neurological diseases.