Lacking of palladin leads to multiple cellular events changes which contribute to NTD

Abstract

BackgroundThe actin cytoskeleton-associated protein palladin plays an important role in cell motility, morphogenesis and adhesion. In mice, Palladin deficient embryos are lethal before embryonic day (E) 15.5, and exhibit severe cranial neural tube and body wall closure defects. However, the mechanism how palladin regulates the process of cranial neural tube closure (NTC) remains unknown.MethodsIn this paper, we use gene knockout mouse to elucidate the function of palladin in the regulation of NTC process.ResultsWe initially focuse on the expression pattern of palladin and found that in embryonic brain, palladin is predominantly expressed in the neural folds at E9.5. We further check the major cellular events in the neural epithelium that may contribute to NTC during the early embryogenesis. Palladin deficiency leads to a disturbance of cytoskeleton in the neural tube and the cultured neural progenitors. Furthermore, increased cell proliferation, decreased cell differentiation and diminished apical cell apoptosis of neural epithelium are found in palladin deficient embryos. Cell cycle of neural progenitors in Palladin -/- embryos is much shorter than that in wt ones. Cell adhesion shows a reduction in Palladin -/- neural tubes.Conclusions Palladin is expressed with proper spatio-temporal pattern in the neural folds. It plays a crucial role in regulating mouse cranial NTC by modulating cytoskeleton, proliferation, differentiation, apoptosis, and adhesion of neural epithelium. Our findings facilitate further study of the function of palladin and the underlying molecular mechanism involved in NTC.Electronic supplementary materialThe online version of this article (doi:10.1186/s13064-017-0081-6) contains supplementary material, which is available to authorized users.

The podocyte-specific knockout of palladin in mice with a 129 genetic background affects podocyte morphology and the expression of palladin interacting proteins

“…In the present study, we have examined the role of the actin-binding and nucleating protein palladin which is important for the organization and stability of the actin cytoskeleton in many cell types [ 8 – 10 ]. An ubiquitous knockout (KO) of palladin in mice is lethal in utero around E15.5 and embryos develop cranial neural tube closure defects [ 10 , 11 ]. Palladin is a scaffold protein consisting of immunoglobulin domains and proline-rich regions that interact with different proteins [ 8 , 12 ] like the vasodilator-stimulated phosphoprotein (VASP) [ 13 ], the LIM and SH3 protein 1 (Lasp-1) [ 14 ] as well as the actin-binding protein α-actinin-1 [ 15 ].…”

Ablation of Tacr2 in mice leads to gastric emptying disturbance

“…Equal amounts of proteins (50‐70 μg) were electrophoresed on 10% SDS‐PAGE and transferred onto nitrocellulose filter membrane (GE). After blocked by 5% skim milk, membranes were incubated with primary antibodies listed in Table S2 overnight at 4°C . To visualize specific protein signals, the secondary antibodies conjugated with IRdye800CW (LI‐COR, Lincoln, USA) were used and the membranes were scanned by Odyssey Infrared Imager (LI‐COR).…”

Cytoskeletal Protein Palladin in Adult Gliomas Predicts Disease Incidence, Progression, and Prognosis

“…In the CNS, palladin is expressed in the neural plate, neural progenitor cells, cortical neurons, and astrocytes [ 38 , 39 , 40 ]. The protein is involved in embryonic development, neuronal maturation, the cell cycle, differentiation, and apoptosis [ 38 , 41 , 42 , 43 ]. The role of palladin in brain tumors is currently unknown.…”