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Creativity Motivation – What is motivation – Corey K Katir
Advertising From http://www.creativitymotivation.com Describes motivation process for creativity with emphasis on intrinsic motivation by Corey K Katir TBX5 intragenic duplication: a family with an atypical HoltaOram syndrome phenotype
From feeds.nature
Hereditary mixed polyposis syndrome is caused by a 40-kb upstream duplication that leads to increased and ectopic expression of the BMP antagonist GREM1
From feeds.nature Ian Tomlinson and colleagues identify a 40-kb duplication upstream of the gene that encodes the BMP antagonist GREM1 in families with hereditary mixed polyposis syndrome. The mutation is associated with increased allele-specific and ectopic expression of GREM1.
A duplicated gene shaped human brain evolutiona| and why the genome project missed it | Not Exactly Rocket Science
From feedproxy.google
Two groups led by Evan Eichler and Franck Polleux have found that humans, alone among all animals, have three extra copies of a gene called SRGAP2, which is involved in brain development. The second of these copies, SRGAP2C, is particularly interesting because it affects the development of neurons, and produces features that are distinctively human. It also emerged between 2 and 3 million years ago, during the time when our brains became much bigger.
Genes are often duplicated by mistake when DNA is copied or shuffled around. These duplications provide raw fuel for fast evolution. Suddenly, genes get back-up copies. Either the original or the duplicate can mutate with impunity and take on new roles. But duplications …
KCTD13 is a major driver of mirrored neuroanatomical phenotypes of the 16p11.2 copy number variant
From feeds.nature Copy number variants (CNVs) are major contributors to genetic disorders. We have dissected a region of the 16p11.2 chromosomeawhich encompasses 29 genesathat confers susceptibility to neurocognitive defects when deleted or duplicated. Overexpression of each human transcript in zebrafish embryos identified KCTD13 as the sole message capable of inducing the microcephaly phenotype associated with the 16p11.2 duplication, whereas suppression of the same locus yielded the macrocephalic phenotype associated with the 16p11.2 deletion, capturing the mirror phenotypes of humans. Analyses of zebrafish and mouse embryos suggest that microcephaly is caused by decreased proliferation of neuronal progenitors with concomitant increase in apoptosis in the developing brain, whereas macrocephaly arises by increased proliferation and no changes in apoptosis. A role for KCTD13 dosage changes is consistent with autism in both a recently reported family with a reduced 16p11.2 deletion and a subject reported here with a complex 16p11.2 rearrangement involving de novo structural alteration of KCTD13. Our data suggest that KCTD13 is a major driver for the neurodevelopmental phenotypes associated with the 16p11.2 CNV, reinforce the idea that one or a small number of transcripts within a CNV can underpin clinical phenotypes, and offer an efficient route to identifying dosage-sensitive loci.
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The Human Genome Project was officially completed in 2003, but our version of the genome is far from truly complete. Scientists are still finishing the last parts, correcting errors in the official sequence, and discovering new genes. These new genes did not go unnoticed because they are useless or insignificant. Some of them may be key players in our evolutionary story.
Capital Online Revenue Introduces Innovate Business Education Techniques
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