A new preprint titled “Legacy Data Confounds Genomics Studies” is recently posted in biorxiv. It shows that the researchers using data from 1000-genome project need to be cautious about garbage-in-garbage-out effect (technical term: batch effect) leading to spurious discoveries.
We are continuing our discussion of eukaryotic genome evolution based on Dan Graur’s “Molecular and Genome Evolution”. In this post, we present a number of puzzling observations in various eukaryotic genomes. The title of each section also includes the page number of Graur’s book, where the observation is reported.
In the previous post, I wrote about the book “Molecular and Genome Evolution” by Dan Graur. It contains thirteen chapters as shown below. Chapters 7-11 may be considered the heart of the book, where Graur discusses how the genomes evolve and how new genes come into existence. Among those, the chapters 6-8 present three mechanisms for genome evolution, namely DNA duplication, molecular tinkering and mobile elements. Subsequently, chapters 10 and 11 discuss evolutionary aspects of the prokaryotic and the eukaryotic genomes respectively.
Over the last two weeks, I have been reading Dan Graur’s book titled “Molecular and Genome Evolution”. This is a fantastic book that everyone should read before starting to work on any genome-related project. For the benefit of our readers, I will share some comments in this short post. If time permits, I will later follow up with a longer post on the book.
‘Ancient’ Bene Israel Jews and late-arrived Baghdadi Jews in India started the
Bollywood movie industry. Many famous early Indian actresses also came from
these communities. This is not common knowledge in India, because those
actresses took Muslim (Firoza Begum) or Hindu (Sulochana, Pramila) screen
Among all biomolecules within the cell, tRNAs got the least respect. Their
supposed importance ended right after the ‘adaptors’ related to entries in the
genetic code table were identified (mid-60s). Since then, the attention
shifted to more complex RNAs like the rRNAs.
Among various biotechnology inventions of the last few years with potential to
revolutionize medicine, nothing excites us more than growing of three-
dimensional human organoids on matrigel. Therefore, we plan to devote a number
of posts on this topic to keep our readers aware of the practices, potentials
How did life originate on earth? What chemical properties of living objects
make them different from the non-living objects? Where did the genome come
from in the first place? How was life before the emergence of the genetic
code? Why does the genetic code have that specific form? What biochemical
advantages do the proteins get by having methionine as their first amino acid?
How did the metabolic pathway evolve to its current form? How did bacteria,
archaea and eukaryotes evolve into distinct kingdoms? How did multi-
cellularity evolve? How did our ability to hear and smell evolve? Where did
the adaptive immune system come from?
These days, when we analyze transcriptome data sets from vetebrates, one or
other solute carrier gene often comes to the top. If have the same experience
and spend a lot of time searching through various databases to find what they
do, the following two reviews will come handy. The first author of both papers
is Matthias A. Hediger, who is currently at Institute of Biochemistry and
Molecular Medicine, University of Bern, Switzerland.
A mitochondrial tRNA(Lys) gene mutation at nucleotide position 8344 is
responsible for the myoclonus epilepsy associated with ragged-red fibers
(MERRF) subgroup of mitochondrial encephalomyopathies. Here, we show that
normally modified uridine at the anticodon wobble position remains unmodified
in the purified mutant tRNA(Lys). We have reported a similar modification
defect at the same position in two mutant mitochondrial tRNAs(Leu)(UUR) in
another subgroup, mitochondrial myopathy, encephalopathy, lactic acidosis and
stroke-like episodes (MELAS), indicating this defect is common in the two
kinds of tRNA molecules with the respective mutations of the two major
mitochondrial encephalomyopathies. We therefore suggest the defect in the
anticodon is responsible, through the translational process, for the
pathogenesis of mitochondrial diseases.
Agmatidine (2-agmatinylcytidine, symbol C+ or agm2C) is a modified cytidine
present in the wobble position of the anticodon of several archaeal AUA
decoding tRNAs. Agmatidine is essential for correct decoding of the AUA codon
in many archaea and is required for aminoacylation of tRNAIle2 with
Agmatidine - wiki