Clueless regulates aPKC activity and promotes self-renewal cell fate in Drosophila lgl mutant larval brains

Goh, Li Hui; Zhou, Xin; Lee, Mei Chin; Lin, Shuping; Wang, Huashan; Luo, Yan; Yang, Xiaohang

doi:10.1016/j.ydbio.2013.06.031

Cited by 18 publications

(15 citation statements)

References 38 publications

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“…FRIENDLY appears to perform a variety of functions (13,20,21). The indistinguishable photorelocation of chloroplasts that we observed in wild type and rec1-3 rec2 rec3-1 friendly and the localization of REC1 to both the cytosol and the nucleus conflict with the idea that REC proteins directly contribute to the tracking of chloroplasts along the cytoskeleton.…”

Section: Discussioncontrasting

confidence: 74%

“…Loss-of-function alleles of FRIENDLY and its orthologs in Dictyostelium discoideum, Saccharomyces cerevisiae, and Drosophila melanogaster cause mitochondrial clustering (19). FRIENDLY and orthologous proteins were reported to perform a variety of functions, such as binding and regulating atypical protein kinase C (20), binding mRNAs that encode mitochondrial proteins and promoting the biogenesis of mitochondria (21), and promoting intermitochondrial associations before mitochondrial fusion (13). The calculated masses of the proteins that are encoded by At4g28080, At1g15290, and FRIENDLY are 200 kDa, 180 kDa, and 150 kDa, respectively.…”

Section: Resultsmentioning

confidence: 99%

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REDUCED CHLOROPLAST COVERAGE genes from Arabidopsis thaliana help to establish the size of the chloroplast compartment

Larkin

Stefano

Ruckle

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Eukaryotic cells require mechanisms to establish the proportion of cellular volume devoted to particular organelles. These mechanisms are poorly understood. From a screen for plastid-to-nucleus signaling mutants in Arabidopsis thaliana, we cloned a mutant allele of a gene that encodes a protein of unknown function that is homologous to two other Arabidopsis genes of unknown function and to FRIENDLY, which was previously shown to promote the normal distribution of mitochondria in Arabidopsis. In contrast to FRIENDLY, these three homologs of FRIENDLY are found only in photosynthetic organisms. Based on these data, we proposed that FRIENDLY expanded into a small gene family to help regulate the energy metabolism of cells that contain both mitochondria and chloroplasts. Indeed, we found that knocking out these genes caused a number of chloroplast phenotypes, including a reduction in the proportion of cellular volume devoted to chloroplasts to 50% of wild type. Thus, we refer to these genes as REDUCED CHLOROPLAST COVERAGE (REC). The size of the chloroplast compartment was reduced most in rec1 mutants. The REC1 protein accumulated in the cytosol and the nucleus. REC1 was excluded from the nucleus when plants were treated with amitrole, which inhibits cell expansion and chloroplast function. We conclude that REC1 is an extraplastidic protein that helps to establish the size of the chloroplast compartment, and that signals derived from cell expansion or chloroplasts may regulate REC1.chloroplast coverage | chloroplast | plastid signaling | chlorophyll | Arabidopsis C hloroplasts drive plant growth, development, and reproduction by converting solar energy into biologically useful forms of energy. Thus, the biogenesis and function of chloroplasts underpin crop yields and, indeed, life on Earth. Chloroplasts develop from proplastids during germination and leaf development (1). After chloroplast biogenesis, chloroplasts divide by binary fission.

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Section: Discussioncontrasting

confidence: 74%

Section: Resultsmentioning

confidence: 99%

REDUCED CHLOROPLAST COVERAGE genes from Arabidopsis thaliana help to establish the size of the chloroplast compartment

Larkin

Stefano

Ruckle

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Adsorption assays in which the antibody was preincubated with the immunogenic peptide demonstrated the specificity of the polyclonal anti-PKA α-subunit [18]. Studies using antibodies obtained from the source we used reported only single bands in Western blots, where PKCα, PKCε, PKCλ or PKCζ were among the protein kinases of interest [19][20][21][22].…”

Section: Methodsmentioning

confidence: 98%

Altered signaling pathways linked to angiotensin II underpin the upregulation of renal Na+-ATPase in chronically undernourished rats

Silva

Muzi‐Filho

Pereira‐Acácio

et al. 2014

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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This study has investigated the participation of altered signaling linked to angiotensin II (Ang II) that could be associated with increased Na(+) reabsorption in renal proximal tubules during chronic undernutrition. A multideficient chow for rats (basic regional diet, BRD) was used, which mimics several human diets widely taken in developing countries. The Vmax of the ouabain-resistant Na(+)-ATPase resident in the basolateral membranes increased >3-fold (P<0.001) accompanied by an increase in Na(+) affinity from 4.0 to 0.2mM (P<0.001). BRD rats had a >3-fold acceleration of the formation of phosphorylated intermediates in the early stage of the catalytic cycle (in the E1 conformation) (P<0.001). Immunostaining showed a huge increase in Ang II-positive cells in the cortical tubulointerstitium neighboring the basolateral membranes (>6-fold, P<0.001). PKC isoforms (α, ε, λ, ζ), Ang II type 1 receptors and PP2A were upregulated in BRD rats (in %): 55 (P<0.001); 35 (P<0.01); 125, 55, 11 and 30 (P<0.001). PKA was downregulated by 55% (P<0.001). With NetPhosK 1.0 and NetPhos 2.0, we detected 4 high-score (>0.70) regulatory phosphorylation sites for PKC and 1 for PKA in the primary sequence of the Na(+)-ATPase α-subunit, which are located in domains that are key for Na(+) binding and catalysis. Therefore, chronic undernutrition stimulates tubulointerstitial activity of Ang II and impairs PKC- and PKA-mediated regulatory phosphorylation, which culminates in an exaggerated Na(+) reabsorption across the proximal tubular epithelium.

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“…Interestingly, both clueless and park (drosophila Parkin gene) mutants display similar Parkinsonian phenotypes and mitochondrial defects [279] as well as a similar NB phenotype, namely mislocalized cell fate determinants [281]. Furthermore, aPKC has been previously shown to regulate the neuronal cell fate determinant TRIM32 [272].…”

Section: Parkin (Park2)mentioning

confidence: 99%

Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression

Grand

Gonzalez-Cano

Pavlou

et al. 2014

Cell. Mol. Life Sci.

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Parkinson's disease (PD) is the second most common neurodegenerative disorder, leading to a variety of motor and non-motor symptoms. Interestingly, nonmotor symptoms often appear a decade or more before the first signs of motor symptoms. Some of these non-motor symptoms are remarkably similar to those observed in cases of impaired neurogenesis and several PD-related genes have been shown to play a role in embryonic or adult neurogenesis. Indeed, animal models deficient in Nurr1, Pitx3, SNCA and PINK1 display deregulated embryonic neurogenesis and LRRK2 and VPS35 have been implicated in neuronal development-related processes such as Wnt/bcatenin signaling and neurite outgrowth. Moreover, adult neurogenesis is affected in both PD patients and PD animal models and is regulated by dopamine and dopaminergic (DA) receptors, by chronic neuroinflammation, such as that observed in PD, and by differential expression of wild-type or mutant forms of PD-related genes. Indeed, an increasing number of in vivo studies demonstrate a role for SNCA and LRRK2 in adult neurogenesis and in the generation and maintenance of DA neurons. Finally, the roles of PDrelated genes, SNCA, LRRK2, VPS35, Parkin, PINK1 and DJ-1 have been studied in NSCs, progenitor cells and induced pluripotent stem cells, demonstrating a role for some of these genes in stem/progenitor cell proliferation and maintenance. Together, these studies strongly suggest a link between deregulated neurogenesis and the onset and progression of PD and present strong evidence that, in addition to a neurodegenerative disorder, PD can also be regarded as a developmental disorder.

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Clueless regulates aPKC activity and promotes self-renewal cell fate in Drosophila lgl mutant larval brains

Cited by 18 publications

References 38 publications

REDUCED CHLOROPLAST COVERAGE genes from Arabidopsis thaliana help to establish the size of the chloroplast compartment

REDUCED CHLOROPLAST COVERAGE genes from Arabidopsis thaliana help to establish the size of the chloroplast compartment

Altered signaling pathways linked to angiotensin II underpin the upregulation of renal Na+-ATPase in chronically undernourished rats

Neural stem cells in Parkinson’s disease: a role for neurogenesis defects in onset and progression

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