Abstract
The intermediate filament protein IFA-2 is essential for the structural integrity of the Caenorhabditis elegans epidermis. It is one of the major components of the fibrous organelle, an epidermal structure comprised of apical and basal hemidesmosomes linked by cytoplasmic intermediate filaments that serve to transmit force from the muscle to the cuticle. Mutations of IFA-2 result in epidermal fragility and separation of the apical and basal epidermal surfaces during postembryonic growth. An IFA-2 lacking the head domain fully rescues the IFA-2 null mutant, whereas an IFA-2 lacking the tail domain cannot. Conversely, an isolated IFA-2 head was able to localize to fibrous organelles whereas the tail was not. Taken together these results suggest that the head domain contains redundant signals for IF localization, whereas non-redundant essential functions map to the IFA-2, tail, although the tail is unlikely to be directly involved in fibrous organelle localization.
Highlights
Intermediate filaments (IFs) form stress resistant cytoskeletal networks that reinforce cell structure and transfer force from individual cells to neighboring cells or extra-cellular matrix via junctional complexes, contributing to tissue integrity [1,2,3]
In addition we show that the head domain, but not tail domain of IFA-2 can localize to fibrous organelles (FOs) in the absence of the rod domain
An ifa-2::gfp fusion gene that completely rescues the ifa-2 null mutation nc16 had been previously generated (Table 1; see reference [7]). In these rescued ifa-2(nc16); erIs1 transgenic animals, IFA-2::GFP protein localizes to the epidermal FOs, the uterine seam and touch neurons (Fig. 2, panels A-C; see reference [7])
Summary
Intermediate filaments (IFs) form stress resistant cytoskeletal networks that reinforce cell structure and transfer force from individual cells to neighboring cells or extra-cellular matrix via junctional complexes, contributing to tissue integrity [1,2,3]. They can interact with signaling molecules and potentially regulate signaling pathways [3,4]. Mutations that disrupt cytoplasmic IFs, desmosomes or hemidesmosomes have been shown to result in developmental abnormalities in experimental model systems, including Caenorhabditis elegans where mutation or RNAi disruptions of epidermal IFs result in tissue separation, failure of embryonic elongation and muscle collapse from the body wall [6,7,8].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
