On the break in the single-particle energy dispersions and the `universal' nodal Fermi velocity in the high-temperature copper-oxide superconductors

Recent data from angle-resolved photoemission experiments published by Zhou et al. [Nature, Vol. 423, 398 (2003)] concerning a number of hole-doped copper-oxide-based high-temperature superconductors reveal that in the nodal directions of the underlying square Brillouin zones (i.e. the directions along which the d-wave superconducting gap is vanishing) the Fermi velocities for some finite range of k inside the Fermi sea and away from the nodal Fermi wavevector k_F are to within an experimental uncertainty of approximately 20% the same both in all the compounds investigated and over a wide range of doping concentrations and that, in line with earlier experimental observations, at some characteristic wavevector k_* away from k_F the Fermi velocities undergo a sudden change, with this change (roughly speaking, a finite discontinuity) being the greatest (smallest) in the case of underdoped (overdoped) compounds. In this paper we present a rigorous analysis concerning the implications of these observations. [Short abstract]Comment: 29 pages, 4 postscript figures. Brought into conformity with the published versio

Bax Function in the Absence of Mitochondria in the Primitive Protozoan Giardia lamblia

Bax-induced permeabilization of the mitochondrial outer membrane and release of cytochrome c are key events in apoptosis. Although Bax can compromise mitochondria in primitive unicellular organisms that lack a classical apoptotic machinery, it is still unclear if Bax alone is sufficient for this, or whether additional mitochondrial components are required. The protozoan parasite Giardia lamblia is one of the earliest branching eukaryotes and harbors highly degenerated mitochondrial remnant organelles (mitosomes) that lack a genome. Here we tested whether human Bax expressed in Giardia can be used to ablate mitosomes. We demonstrate that these organelles are neither targeted, nor compromised, by Bax. However, specialized compartments of the regulated secretory pathway are completely ablated by Bax. As a consequence, maturing cyst wall proteins that are sorted into these organelles are released into the cytoplasm, causing a developmental arrest and cell death. Interestingly, this ectopic cargo release is dependent on the carboxy-terminal 22 amino acids of Bax, and can be prevented by the Bax-inhibiting peptide Ku70. A C-terminally truncated Bax variant still localizes to secretory organelles, but is unable to permeabilize these membranes, uncoupling membrane targeting and cargo release. Even though mitosomes are too diverged to be recognized by Bax, off-target membrane permeabilization appears to be conserved and leads to cell death completely independently of mitochondria

Expression of a rice chitinase gene in transgenic banana ('Gros Michel', AAA genome group) confers resistance to black leaf streak disease

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