On the cover
Tropomodulin1 (green) is required for the regular hexagonal packing of mouse lens fiber cells, binding to a sub population of F-actin (red) that connects a spectrin-based network underlying the cell membranes. See page 915.
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Role of ERO1-α–mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress–induced apoptosis
CHOP turns on ERO1-α to release calcium via IP3R and trigger cell death in response to ER stress.
The soluble and membrane-anchored isoforms of Mgm1 are only active when they work together (in trans).
Brain-specific Drp1 knockout mice demonstrate that Drp1-mediated organelle division is important for development, mitochondrial morphogenesis, and apoptosis.
Regulation of dynein-driven microtubule sliding by the axonemal protein kinase CK1 in Chlamydomonas flagella
CK1 puts the brakes on dynein activity when added to purified axonemes in vitro, presumably to regulate how flagella bend.
Nucleotide excision repair–induced H2A ubiquitination is dependent on MDC1 and RNF8 and reveals a universal DNA damage response
The epigenetic mark indicative of DNA UV damage or double-strand breaks is achieved via a common pathway regardless of the cause of damage.
Ribosome stalk assembly requires the dual-specificity phosphatase Yvh1 for the exchange of Mrt4 with P0
The step by step assembly process from preribosome in the nucleus to translation-competent 60S ribosome subunit in the cytoplasm is revealed (also see Kemmler et al. in this issue).
The step by step assembly process from preribosome in the nucleus to translation-competent 60S ribosome subunit in the cytoplasm is revealed (also see Lo et al. in this issue).
Uncoordinated movement in Rab2 mutants is caused by impaired retention of cargo on dense core vesicles, not by defective synaptic vesicle release. (Also see the companion article by Sumakovic et al. in this issue.)
UNC-108/RAB-2 and its effector RIC-19 are involved in dense core vesicle maturation in Caenorhabditis elegans
Uncoordinated movement in Rab2 mutants is caused by impaired retention of cargo on dense core vesicles, not by defective synaptic vesicle release. (Also see the companion article by Edwards et al. in this issue.)
Tropomodulin1 is required for membrane skeleton organization and hexagonal geometry of fiber cells in the mouse lens
The spectrin–actin network is disrupted in Tmod1 mutants, disturbing fiber cell morphology, and disordering lens cell organization.