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Cytoplasmic poly (A)-binding protein critically regulates epidermal maintenance and turnover in the planarian Schmidtea mediterranea.


ABSTRACT: Identifying key cellular events that facilitate stem cell function and tissue organization is crucial for understanding the process of regeneration. Planarians are powerful model system to study regeneration and stem cell (neoblast) function. Here, using planaria, we show that the initial events of regeneration, such as epithelialization and epidermal organization are critically regulated by a novel cytoplasmic poly A-binding protein, SMED-PABPC2. Knockdown of smed-pabpc2 leads to defects in epidermal lineage specification, disorganization of epidermis and ECM, and deregulated wound healing, resulting in the selective failure of neoblast proliferation near the wound region. Polysome profiling suggests that epidermal lineage transcripts, including zfp-1, are translationally regulated by SMED-PABPC2. Together, our results uncover a novel role for SMED-PABPC2 in the maintenance of epidermal and ECM integrity, critical for wound healing and subsequent processes for regeneration.

SUBMITTER: Bansal D 

PROVIDER: S-EPMC5611960 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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Cytoplasmic poly (A)-binding protein critically regulates epidermal maintenance and turnover in the planarian <i>Schmidtea mediterranea</i>.

Bansal Dhiru D   Kulkarni Jahnavi J   Nadahalli Kavana K   Lakshmanan Vairavan V   Krishna Srikar S   Sasidharan Vidyanand V   Geo Jini J   Dilipkumar Shilpa S   Pasricha Renu R   Gulyani Akash A   Raghavan Srikala S   Palakodeti Dasaradhi D  

Development (Cambridge, England) 20170814 17


Identifying key cellular events that facilitate stem cell function and tissue organization is crucial for understanding the process of regeneration. Planarians are powerful model system to study regeneration and stem cell (neoblast) function. Here, using planaria, we show that the initial events of regeneration, such as epithelialization and epidermal organization are critically regulated by a novel cytoplasmic poly A-binding protein, SMED-PABPC2. Knockdown <i>of smed-pabpc2</i> leads to defects  ...[more]

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