I recommend considering all clauses, subclauses, definitions etc. If you're interested, here's a link to the bill itself, showing amendments that have been made in response to issues raised by both MPs and members of the public (this article was also published on the same day on StuffNZ with the headline "Food Bill threatens 'bake sales'" - take from that what you will.) In addition there have been several recent news articles/press releases by Green MPs about the bill and common misconceptions about it (some of which continue to be disseminated by the author of the below petition): Before considering signing, please take the time to read the Q&A on the MAF website addressing concerns that have already been raised about the bill. (D) Sequence traces of C8orf38 from each family member in (A) and one healthy control demonstrating homozygosity for a c.296A>G mutation in both affected siblings.I've seen the link to the "Oppose the NZ Food Bill 160-2" come up on my feed with increasing frequency in the past month or two (link below). Eight intervals of homozygosity shared by the affected siblings but not the parents or unaffected sibling are listed along with the number of genes in various categories for each interval (CI, known complex I genes COPP, Complex One Phylogenetic Profiling candidates). (C) Results of homozygosity mapping using DNA from family members in (A). The final column lists citrate synthase activities (relative to total protein) as % of normal control mean (see Experimental Procedures).
(B) Respiratory chain enzyme activities, standardized against the mitochondrial matrix marker enzyme citrate synthase, expressed as percentages of the mean value (normal ranges in parentheses).
Letters beneath each family member represent the genotype for a c.296A>G mutation in C8orf38. (A) Pedigree from a consanguineous Lebanese family with two children affected by Leigh syndrome and complex I deficiency. Error bars represent the range of duplicate assays. (F) CI activity assays from fibroblast lysates (as in D) for controls (gray bars) and four candidates (blue bars). (E) Percent knockdown of mRNA expression achieved for controls (gray bars) or CI candidates (blue bars) as measured by real-time qPCR. Immunoblots of actin and a CI subunit from whole cell lysates were performed following lentiviral-mediated delivery of an empty vector or hairpins targeted against GFP (negative control), NDUFAF1 (known CI assembly factor) and four CI candidates. (D) Effect of candidate knockdown on CI levels in human fibroblasts.
(C) Reconstructed phylogenetic eukaryotic tree, with red text indicating species that have lost CI. Asterisks indicate candidates tested by RNAi in (D-F). (B) MitoCarta proteins matching the phylogenetic profile of the subset of CI subunits lost independently at least four times in evolution. Blue squares indicate homology of the mouse protein (row) to a protein in a target species (column). (A) Presence/absence matrix for 44 respiratory chain CI subunits and 3 assembly factors across 42 eukaryotic species. Our results have important implications for understanding CI function and pathogenesis and, more generally, illustrate how our compendium can serve as a foundation for systematic investigations of mitochondria. We validate a subset of these predictions using RNAi, including C8orf38, which we further show harbors an inherited mutation in a lethal, infantile CI deficiency. Using this approach, we predict 19 proteins to be important for the function of complex I (CI) of the electron transport chain. We link poorly characterized proteins in this inventory to known mitochondrial pathways by virtue of shared evolutionary history. Toward this goal, we performed mass spectrometry, GFP tagging, and machine learning to create a mitochondrial compendium of 1098 genes and their protein expression across 14 mouse tissues. Identifying all of the proteins resident in this organelle and understanding how they integrate into pathways represent major challenges in cell biology. Mitochondria are complex organelles whose dysfunction underlies a broad spectrum of human diseases.
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