Color Mutations

A comprehensive investigation in guppy color biology, pattern formation and a unique hypothesis about the biological basis for guppy polymorphism. Includes chapters reviewing relevant animal pattern research. Includes information about the author's experiments using classical forward genetics.

THIS IS REALLY QUITE AMAZING AS TO HOW RIGHT ON, THIS PAINTING BY BEV IS, WITH WHAT ALREADY IS IN THE EUPHORIC PURPLISH GRAY BOUNDARY LAYER.  EVEN THE GOD PARTICLE HAS TO CHANGE SHAPE AS SHE SHOWS US – THENCE, THE GOD PARTICLE FUNCTION HAS TO CHANGE!!!

NOW THERE'S PAINTINGS BY BRIDGET THAT DEPICT A NEW SOUL COALESCING IN THE PURPLISH GRAY BOUNDARY LAYER.  AT THE END OF THE ESSAY

AND THERE IS ONE PHOTO THAT  CONFIRMS THE ESSAY AND THAT WHAT BRIDGET SEES ARE REALITY.

BECAUSE THE SUN ITSELF IS EMANATING THE COLOR LT PURPLE.

EUPHORIA REALLY IS A HUGE DEAL. 

MASSIVE CHANGE - THE ENTIRE COLOR SPECTRUM!!! IT IS HAPPENING NOW.  AND IT HAS HAPPENED BEFORE!!!  ANCIENT EARTH WAS LT. PURPLE!! 
https://www.livescience.com/1398-early-earth-purple-study-suggests.html

The article is a group effort consisting of an introduction and seven compact essays. It is focused on the problem of color from the perspective of current philosophical discussions on the role of the Enlightenment and the relationship between light and dark. The introduction by Michael Kurtov presents a roadmap for navigating through the seven essays by referring to a schema of “color knowledge” which has four dimensions: luminosity, resolution, saturation, and hue. Each of the texts in the article (the introduction and seven essays) deals mostly with one of “color knowledge”, which are formed by combining three color dimensions. Roman Mikhailov explores the plastic-dynamic correlates of colors and the chromaticity of the text understood broadly both as the text of nature and as an abstract symbolic complex. Eugene Kuchinov offers a “haptic criticism of the Enlightenment,” which is an analysis of color phenomena from the point of view of the skin (not the eye): on the basis of the logic of sensation, color is “viewed” beyond the light, beyond the optics. Yoel Regev develops a hermeneutics of color applied to the Torah: color is interpreted as a deception which is opposed to another deception belonging to a “true enlightenment.” Michael Kurtov addresses a revision of Goethe’s theory of color based on new physical experiments and on the logical geometry of color and then arrives at a critique of contemporary chromo-ideology. Nataliya Tyshkevich reveals the modern political meaning of coloring in the context of the recent “renaissance of modernist aesthetics” in which dealing with form is replaced by dealing with surfaces. Gray Violet describes color and darkness as political functions that turn into each other in the middle of a non-place in the “smart city.” The final piece by Nikita Sazonov elaborates the procedure of colorization by examining noncolor — a resource beyond the colored and the uncolored, most readily manifested in the printed character as well as in modern hip-hop culture
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Статья представляет собой коллективный текст, состоящий из введения и семи фрагментов. В центре статьи — проблема цвета, рассмотренная сквозь призму актуальных философских дискуссий о роли Просвещения и отношениях «светлого» и «темного». Во введении Михаила Куртова предлагается общая карта движения по семи фрагментам — модель «цветного знания», имеющая четыре измерения: светлота, разрешение, насыщенность, цветовой тон. Каждый из включенных в статью текстов (введение и семь фрагментов) условно отнесен к одному из восьми возможных типов «цветного знания». Фрагмент Романа Михайлова исследует пластически-динамические корреляты цветов и говорит о цветности текста, понимаемого максимального широко: и как текста природы, и как абстрактного символического комплекса. Фрагмент Евгения Кучинова посвящен «гаптической критике Просвещения» — анализу цвета с точки зрения «кожи», располагающемуся на границе оптического как такового и получающему свой смысл в интенсивном, аффективно-динамическом знании. Фрагмент Йоэля Регева разворачивает герменевтику цвета на материале Торы: цвет истолковывается как обман, которому противостоит другой обман, принадлежащий «подлинному просвещению». Фрагмент Михаила Куртова обращается к пересмотру теории цвета Гёте на базе новых физических экспериментов и с учетом развития логической геометрии цвета, намечая тем самым критику современной хромоидеологии. Фрагмент Натальи Тышкевич раскрывает современный политический смысл раскрашивания в контексте «ренессанса модернистской эстетики» последних лет, в которой работа с формой замещается работой поверхностями. Фрагмент Серого Фиолетового описывает цвет и тьму как политические функции, обращающиеся друг в друга посреди единого не-места «умного города». Заключительный фрагмент Никиты Сазонова разрабатывает процедуру расцвечивания через обращение к нецвету — ресурсу по ту сторону цвета и не-цвета, наиболее отчетливо проявляющемуся в печатном знаке, а также в современной хип-хоп культуре

SUMMARY Peach flesh color (white or yellow) is among the most popular commercial criteria for peach classification, and has implications for consumer acceptance and fruit nutritional quality. Despite the increasing interest in improving cultivars of both flesh types, little is known about the genetic basis for the carotenoid content diversity in peach. Here we describe the association between genotypes at a locus encoding the carotenoid cleavage dioxygenase 4 (PpCCD4), localized in pseudomolecule 1 of the Prunus persica reference genome sequence, and the flesh color for 37 peach varieties, including two somatic revertants, and three ancestral relatives of peach, providing definitive evidence that this locus is responsible for flesh color phenotype. We show that yellow peach alleles have arisen from various ancestral haplotypes by at least three independent mutational events involving nucleotide substitutions, small insertions and transposable element insertions, and that these mutations, despite being located within the transcribed portion of the gene, also result in marked differences in transcript levels, presumably as a consequence of differential transcript stability involving nonsense-mediated mRNA decay. The PpCCD4 gene provides a unique example of a gene for which humans, in their quest to diversify phenotypic appearance and qualitative characteristics of a fruit, have been able to select and exploit multiple mutations resulting from a variety of mechanisms.

Cleft lip and/or cleft palate is one of the most common congenital malformation in
humans that prevelance is a 1-500/1000 worldwide and 0.95/1000 in Turkish
individuals. The etiology of diease is multifactorial, which is combined of genetic and
enviromental factors. Nonsyndromic cleft lip and/or cleft palate has a higher prevalence,
approximately 70% higher than the syndromic type. Numerous candidate genes
determinated as a cause of nonsyndromic CL/P. The aim of the present study is to
define some polimorphisms of mutations in IRF6 and MSX1 genes and to investigate
the prevalence in the Turkish nonsyndromic cleft lip and palate population. In our
research, we compare 71 unrelated nonsyndromic CL/P cases and 89 unrelated control
indivuduals in case-control study. -8796A>G ve 820 G>A polymorphisms in MSX1 and
IRF6 genes were analyzed by PCR-PFLP technique, respectively. -8796A>G
polymorphism (p=0.008849) of the MSX1 gene is a common cause for cleft occurence
in Turkish nonsyndromic CL/P patient unlike IRF6 820GÆA polymorphism(p=1).

Cancer evolves as a result of an accumulation of mutations and chromosomal aberrations. Developments in sequencing technologies have enabled the discovery and cataloguing of millions of such mutations. The identification of protein-level alterations, typically by using reversed-phase protein arrays or mass spectrometry, has lagged, however, behind gene and transcript-level observations. In this study, we report the use of mass spectrometry for detecting the presence of mutations-missense, indels and frame shifts-in MCF7 and SKBR3 breast cancer, and non-tumorigenic MCF10A cells. The mutations were identified by expanding the database search process of raw mass spectrometry files by including an in-house built database of mutated peptides (XMAn-v1) that complemented a minimally redundant, canonical database of Homo sapiens proteins. The work resulted in the identification of nearly 300 mutated peptide sequences, of which ~50 were characterized by quality tandem mass spectra. We describe the criteria that were used to select the mutated peptide sequences, evaluate the parameters that characterized these peptides, and assess the artifacts that could have led to false peptide identifications. Further, we discuss the functional domains and biological processes that may be impacted by the observed peptide alterations, and how protein-level detection can support the efforts of identifying cancer driving mutations and genes. Mass spectrometry data are available via ProteomeXchange with identifier PXD014458. Cancer develops as a result of genetic alterations that include mutations and chromosomal abnormalities. Mutations include alterations such as single nucleotide substitutions (missense, nonsense and silent) and small insertions, deletions or frameshifts. Chromosomal abnormalities can be numerical, i.e., manifest themselves either as gains or losses in chromosome numbers (aneuploidy), or structural, i.e., lead to rearrangements such as translocations, inversions, deletions, insertions or duplications. Comprehensive high-throughput sequencing efforts have revealed a complex interplay of aberrations that define the heterogeneous nature of cancer genomes. Earlier studies have identified ~140 genes that drive tumorigenesis, when altered by mutations 1. These genes regulate three essential cellular processes through twelve signaling pathways, i.e., genome maintenance, cell survival and cell fate. Depending on type, tumors can harbor from 1-2 to 8 driver mutations that generally contribute to the development of cancer over 20-30 years in adults 1. The field of cancer genomics, supported by the advance of sequencing technologies, has witnessed, however, a remarkable growth in the past decade, leading to joint multi-institutional efforts aimed at creating comprehensive resources that encompass hundreds to thousands of gene alterations with potential diagnostic and prognostic significance. Some of these resources include the Wellcome Sanger Institute's COSMIC (Catalogue of Somatic Mutations in Cancer) and CGC (Cancer Gene Census) databases 2 , the cancer-specific projects supported by the International Cancer Genome Consortium (ICGC) 3 , the Cancer Cell Line Encyclopedia (CCLE) 4 , and the PanCancer Atlas project conducted by The Cancer Genome Atlas (TCGA) collaboration 5. With millions of documented mutations, efforts have shifted towards advancing lists of specific cancer driver genes and mutations. On the line of such efforts, the OncoKB-a precision oncology knowledge database-has expanded the number of cancer genes to 1,019, highlighting actionable alterations 6 , while the CGC has catalogued 719 genes matched to cancer hallmarks and grouped into two tiers (tier 1 with documented activity in cancer, and tier 2 with strong indication of having a role in cancer). Recently, the PanCancer Atlas project reported results that were generated through an effort that encompassed the analysis of

Hereditary hearing loss (HHL) is a very common disorder. When inherited in an autosomal recessive manner, it typically presents as an isolated finding. Interestingly and unexpectedly, in spite of extreme heterogeneity, mutations in one gene, GJB2, are the most common cause of congenital severe-to-profound deafness in many different populations. In this study, we assessed the contributions made by GJB2 mutations and chromosome 13 g.1777179_2085947del (the deletion more commonly known as del (GJB6-D13S1830) that includes a portion of GJB6 and is hereafter called Δ(GJB6-D13S1830)) to the autosomal recessive non-syndromic deafness (ARNSD) genetic load in Iran. Probands from 664 different nuclear families were investigated. GJB2-related deafness was found in 111 families (16.7%). The carrier frequency of the 35delG mutation showed a geographic variation that is supported by studies in neighboring countries. Δ(GJB6-D13S1830) was not found. Our prevalence data for GJB2-related deafness reveal a geographic pattern that mirrors the south-to-north European gradient and supports a founder effect in southeastern Europe. © 2005 Wiley-Liss, Inc.