Exact(4)
Two main hypotheses have been proposed to explain this apparent paradox: the 'concerted evolution' hypothesis and the 'evolution by birth and death' hypothesis.
Our results are in agreement with the "birth and death hypothesis" for the evolution of C2H2-ZNF genes, but also show that this hypothesis alone cannot explain the considerable evolutionary variation within the subfamilies of these genes in mammals.
The evolution by birth and death hypothesis, on the other hand, proposes that strong homologies among MHC class I genes within a species can only arise when the entire class I gene pool re-evolves from a single sequence by successive gene duplications [ 11, 12, 17- 19].
The birth and death hypothesis as previously described [ 48, 49] with a relaxed purifying selection favouring multiple amino-acid changes explains the large repertoire of ORs found in numerous species [ 11– 14] as well as their partition in many families and subfamilies.
Similar(56)
This result casts doubt on the growth control and programmed cell death hypotheses.
Since the 'concerted evolution' and the 'birth and death' hypotheses are not mutually exclusive, our results are in agreement with a model where both phenomena contribute to the homology of MHC molecules observed within species.
Although it was initially thought that autophagy was responsible for a form of cell death, this hypothesis has been revised in light of a large body of evidence supporting autophagy as a prosurvival mechanism (Levine and Kroemer, 2009).
In a paper published last month in the journal Palaeobiodiversity and Palaeoenvironments, Achim G. Reisdorf of the University of Basel in Switzerland writes that the trouble with the death-throe hypothesis is that carcasses are flexible.
In conclusion, our findings support the death-dip hypothesis.
The continued plausibility of the death-induced hypothesis of CSF-tau in AD appears to be based on analogy with episodic conditions (head trauma, stroke, severe seizures) in which the time course of CSF or blood tau levels can be measured relative to a single generative event.
Although the disease is well-known and causes severe consequences such as early embryo death, contradictory hypotheses have been made around its etiology, the more supported being a malfunctioning of the immune system and a dysregulation of the inflammatory processes [ 16].
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