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Contents:
  1. Dream Theater
  2. ROUGE VOLUPTÉ SHINE OIL-IN-STICK
  3. ‎A Change of Hearts - The Pink Collection 61 (Unabridged) on Apple Books

Interestingly, no protein expression was detected from the intron 6-insertion construct, possibly due to mRNA instability caused by retention of the intron Fig. This finding correlated well with the observation that full-length TAMM41 transcripts were missing in Patient 26 and Patient The partial intron 7-containing transcript from patient introduced a premature stop codon, leading to the generation of a truncated TAMM41 protein Fig.

Through genetic mapping of 3p-deletion patients, a critical missing region which confers susceptibility for the development of CHD has been determined [ 10 , 11 , 13 ]. However, confounding factors such as incomplete penetrance and long-range regulatory effects have made it difficult to precisely determine the causative genes [ 12 , 14 , 15 ]. Indeed, patients with large deletions of 3p but with normal phenotypes have also been reported [ 36 ]. All three patients manifested abnormally spliced and significantly reduced expression of normal TAMM41 transcripts.

Intriguingly, the biological father of Patient had no obvious heart disease and TAMM41 expression levels remained normal. However, since few imprinting genes were identified, their contributions to the incomplete penetrance of CHD might be minor.

As such, we favor the more widely reported phenomenon of monoallelic expression MAE. MAE, an important regulatory mechanism for cellular heterogeneity and incomplete penetrance observed in multiple genetic diseases, occurs in specific cell types and shows temporal regulation [ 34 ]. Within heart tissue, preferential expression of imprinted genes from the paternal allele has previously been reported. Hence, it would not be surprising if a similar preference for monoallelic gene expression as demonstrated here in TAMM41 mutant patients , also existed.

After the initial discovery of mitophagy in erythrocyte maturation, it has now been shown to participate in multiple biological processes, for instance, sperm motility and viability, midgut metamorphosis, and maintenance of stem cell pluripotency [ 39 , 40 , 41 ]. In adult hearts, mitophagy acts more as an inducible sensor against stress or injury [ 42 ].

However, investigations of the role of mitophagy during embryonic heart development using genetically modified mouse models have often been hampered by early lethality or functional compensation due to induction of ancillary or redundant pathways [ 42 , 43 , 44 ]. Indeed, a recent in vivo mitophagy assay using mito-QC found that active mitophagy did occur during mouse embryonic cardiomyocyte development [ 25 ] and furthermore, that autophagy inhibition induced heart valve abnormalities within zebrafish embryos [ 19 ]. The preferential use of a specific mitophagy pathway, for example, NIX activation of mitochondrial elimination in erythrocyte maturation, indicates that tissue or context-specific regulatory mechanisms may exist [ 45 ].

Thus our identification of the requirement of Tammdependent mitophagy for heart valve development improves our understanding of the diversified roles of mitophagy played. It has been found that mitochondria modulate cellular behavior through mechanisms like eradication ROS, metabolic remodeling and so on [ 46 ]. The so induced glycolysis by mitophagy is essential for the differentiation of neurons and macrophages.

Likely, embryonic heart also prefers glycolysis as the main energy source. In our study, we found that in the heart valve formation regions, mitophagosomes were specifically increased and inhibition of mitophagy was sufficient to induce heart valve abnormalities in zebrafish embryos, as revealed by the defects in expression of bmp4 and notch1b in the AV canal.

A Change of Hearts - The Pink Collection 61, Chapter 19.2 - A Change of Hearts - The Pink...

So we postulate that activated mitophagy in myocardium may help to remodel a favorable metabolic environment to facilitate endocardial invasion or trigger specific pathways, for instance, Notch1 activation. Thus future studies are needed for illustrating the precise mechanisms inside. All subjects were of Chinese Han ethnicity. For each patient, medical history was taken, and physical examinations were performed.

The final diagnosis was confirmed by echocardiography, cardiac magnetic resonance, or cardiac catheterization. Sixty-six patients were diagnosed as simple AVSD, with the remainder showing more complex heart abnormalities. Patients with Trisomy 21 were excluded. The maintenance, breeding, and staging of zebrafish were performed as previously described [ 49 ].

After washing twice, the deposited cells were subjected to electron microscopy analysis. A multiplex-PCR based method, as described previously was employed to capture the targeted sequences [ 50 ]. Whole exome sequencing and variant filtering were performed using an Agilent SureSelect V6 enrichment capture kit Agilent Technologies with sequencing on the Illumina HiSeq x10 platform.

Variant discovery and genotype calling of single nucleotide variants SNVs , insertions and deletions were performed on all individuals using Sentieon DNA pipeline. To identify other potential pathogenic variants, the ones with snp Common record were removed. The pathogenic variants were also evaluated using different in silico predictive algorithms like SIFT, Polyphen v2.

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The Tg cmlc2 : GFP line were used as previously described [ 54 ]. F1 embryos carrying potential indel mutations were raised to adulthood. The minigene splicing reporter was constructed as previously reported. Vectors carrying mutant alleles were generated by a PCR-mediated mutagenesis strategy. Opa3-pink1 was cloned as previously described [ 30 ]. Zebrafish tamm41 , pink1 , park2 , dnm1l were amplified from zebrafish cDNA. Tol2-plasmid was cloned by insertion of zebrafish tamm41 CDS under myl7 promoter 1.

Microinjection of morpholino oligonucleotides or mRNA was performed at the one-cell stage. All injections were performed with a Harvard Apparatus micro-injector. Antisense digoxigenin-labeled RNA probes for nkx2. After PBS washing twice, Hoechst Invitrogen were also added for visualizing cell nuclear confocal microscopy. For immunofluorescence assays, dissected hearts after fixing were incubated with primary antibodies overnight after blocking and permeabilization.

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Secondary antibodies were treated for two hours before the examination. Secondary antibodies Invitrogen used were: Alexa Fluor goat anti-rabbit, Alexa Fluor goat anti-rabbit, Alexa Fluor goat anti-mouse, Alexa Fluor goat anti-human. After washing three times with PBS, embryos were then subjected to fluorescence microscopy examination. Zebrafish or cell line mitochondria were isolated using Tissue Mitochondrial Isolation Kit beyotime or Cell Mitochondrial Isolation Kit beyotime , respectively, as instructed.

After each indicated treatment, cells were then fixed with freshly prepared 3. Subsequently, the cells were dehydrated with increasing concentrations of ethanol, and embedded with epoxy resin. AC16 ultrastructures were taken using a transmission electron microscope Hitachi, H, Japan. For zebrafish heart electron microscopy analysis, the same procedures were performed on whole zebrafish embryos and ultra-thin sections of heart tissue were then examined using electron microscope Hitachi, H, Japan.

Zebrafish immunofluorescence staining images were taken using an Olympus FV scanning confocal microscope.

‎A Change of Hearts - The Pink Collection 61 (Unabridged) on Apple Books

Mitochondrial area and content percentage of mitochondrial area compared to the whole-cell area were quantified using ImageJ. For all analysis, images in each group were obtained by uniform random sampling and processed by identical protocols. For each heart, three peri-CMs regions of the similar size with the corresponding valve region were randomly chosen. Parkin aggregation was counted as the number of cells with parkin translocation to mitochondria compared to all the cells. Fully informed consents were obtained from all parents or guardians.

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Am J Hum Genet. Molecular regulation of atrioventricular valvuloseptal morphogenesis. Endocardial cushion tissue development: structural analyses on the attachment of extracellular matrix to migrating mesenchymal cell surfaces. Scan Electron Microsc. Programmed mitophagy is essential for the glycolytic switch during cell differentiation. EMBO J. Autophagy is essential for cardiac morphogenesis during vertebrate development.

The translocator maintenance protein Tam41 is required for mitochondrial cardiolipin biosynthesis. J Cell Biol. Identification of Tam41 maintaining integrity of the TIM23 protein translocator complex in mitochondria. Staudt D, Stainier D. Uncovering the molecular and cellular mechanisms of heart development using the zebrafish. Annu Rev Genet. Inhibition of cytochrome c release by N-nonyl acridine orange, a cardiolipin-specific dye, during myocardial ischemia-reperfusion in the rat.

A sensitive and quantitative technique for detecting autophagic events based on lysosomal delivery.