Published December 11, 2014 Reported in Journals and Conferences on Genetics & Molecular Biology·Wednesday, September 7, 2016
… viral latency is responsible for life-long pathogenesis and mortality risk…
Kallmann syndrome (KS) is characterized by the association of hypogonadotropic hypogonadism and anosmia. The gene underlying the X chromosome-linked form of the disease, KAL-1, consists of 14 coding exons. It encodes a glycoprotein, anosmin-1, which is involved in the embryonic migration of GnRH-synthesizing neurons and the differentiation of the olfactory bulbs.
KS exemplifies the opposite of nutrient energy-dependent viral latency. Constraint breaking mutations link the transgenerational epigenetic inheritance of Zika virus-driven damage to the physiology of pheromone-controlled reproduction in species from microbes to humans via the de novo creation of G protein-coupled receptors and the loss of olfactory receptor genes, which are required for cell type differentiation in the olfactory bulbs.
The most unexpected finding was that about 90 percent of 6,251 novel RNA transcripts identified are not the usual protein-encoding variety at all, but are “long intergenic non-coding RNAs,” aka “LINC RNAs.” They are highly specific to body parts, where they apparently control the deployment of transcription factor proteins, which in turn steer the program of gene activation and suppression that directly oversees the changes of development.
Expected findings already have linked nutrient energy-dependent species-specific LINC RNAs (lncRNAs) from hydrogen-atom transfer in DNA base pairs in solution to the physiology of reproduction and supercoiled DNA via biophysically constrained RNA-mediated amino acid substitutions and protein folding chemistry. Only researchers who have ignored what is known about KS would be among the biologically uninformed masses who think the details reported in the context of genetic choreography had not already been reported in From Fertilization to Adult Sexual Behavior.
A single gene defect, the X-linked KALIG-1, has been linked to adverse effects on the human GnRH axon trajectory associated with Kallmann’s syndrome. This genetic defect also links the embryonic development of the GnRH neuronal system to disordered olfaction and gonadal incompetence (Caviness, 1992). GnRH deficiency without anosmia may reflect a difference in the ability of GnRH neurons to migrate which may result from the interaction of other genes with KALIG-1 (Crowley and Jameson, 1992).
The obvious link to hormone-organized and hormone-activated behavior in species from insects to mammals was reported in Organizational and activational effects of hormones on insect behavior. The authors cited our 1996 review:
Effects of hormones on brain and behavior occur through three mechanisms: (1) behaviors both organized and activated by hormones, (2) behaviors only organized by hormones, and (3) behaviors only activated by hormones (reviewed in Arnold and Breedlove, 1985; Diamond et al., 1996).
The need to link the de novo creation of proteins from ecological variation to ecological adaptation in species from microbes to mammals has been clear for more than 20 years, but evolutionary theorists have reported that new proteins evolve, and linked the evolution of new proteins from effects on hormones to affects on behavior.
…one may view de novo protein-coding gene evolution as a continuum from non-functional genomic sequences to fully-fledged protein-coding genes (Albà and Castresana, 2005; Toll-Riera et al., 2009; Carvunis et al., 2012). Therefore, many lncRNAs could be in intermediate states in this process, their pervasive translation serving as the building material for the evolution of new proteins. It may be difficult to obtain functional proteins from completely random ORFs (Jacob, 1977), but the effect of natural selection preventing the production of toxic peptides (Wilson and Masel, 2011), and the high number of transcripts expressed in the genome, may facilitate this process.
Anyone who has been convinced that energy-dependent behaviors evolve via the creation of new proteins is not likely to look further into what is known to serious scientists about biologically-based cause and effect.
Similar to other co-evolving host—pathogen relationships, honey bee viruses have likely evolved mechanisms to overcome and/or evade bee immune responses.
In conclusion, this is an exciting time in honey bee virology. Important research topics include (1) understanding honey bee antiviral responses, including those triggered by dsRNA and siRNA, at the cellular and molecular levels, and identifying viral counter measures; (2) identifying the most pathogenic virus strains and determining what factors govern their virulence and transmission; (3) investigating the role of the bee microbiome on virus infection and bee health; and (4) determining how synergistic variables, including agrochemical exposure and nutritional stress, impact viral pathogenesis. Further investigation of these and other topics will advance our understanding of bee biology, host—pathogen interactions, colony health, and may lead to the development of strategies that limit colony losses.
The colony losses are due to nutrient stress and/or social stress. All loss of functional proteins is due to virus-driven energy theft under conditions of stress and loss of function can be viewed in the context of what we reported in the molecular epigenetics section of From Fertilization to Adult Sexual Behavior.
The anti-entropic virucidal energy of the sun anti-entropic virucidal energys virus-driven energy theft. But the immune system defenses of species have been overwhelmed by stress, which links viral persistence and mutations to pathology across generations of cell type lineages in species from microbes to humans. Attempts to explain biologically-based cause and effect to theorists or anyone who is biologically uninformed are futile. The pseudoscientific nonsense about mutations, natural selection, and evolution of proteins is pervasive because it has been taught to students since the time neo-Darwinian theories were invented.
No matter how many examples of natural selection for energy-dependent codon usage in all species continue to link RNA-mediated amino acid substitutions to cell type differentiation and also link virus-driven energy theft to all pathology, theorists seem willing to keep touting their pseudoscientific nonsense and many people will continue to believe them. Only among friends is it possible to discuss what I know about energy-dependent top-down causation. Even most of my family members are not willing to discuss what will happen to the colonies of bee-keepers who refuse to limit the stress that contributes to colony collapse.
The honeybee model organism links Zika virus driven pathology from virus-driven energy theft to craniofacial morphology and brain development across generations, which suggests the failure to accept facts about the cause of mutations will lead to the death of us all.