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    Lechtreck et al. reveal that the BBSome complex exports signaling proteins out of cilia. Though phospholipase D (PLD) accumulates in the cilia of Chlamydomonas cells lacking the BBSome subunit BBS4, mating these mutants with wild-type algae generates quadraciliated zygotes (pictured), in which the BBSome's function is restored, leading to the rapid export of PLD (red) from cilia (green) to the cell body.
    Image © 2013 Lechtreck et al.
    See page 249.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Researchers describe technique to identify genomic loci that interact with specific nuclear structures.

People & Ideas

Gardel studies the biophysical properties of cells and cellular force generation.

Review

Report

In contrast to the situation in mammalian oocytes, the metaphase-to-anaphase transition in frog oocytes is not regulated by a spindle assembly checkpoint.

Article

A comprehensive survey of the roles of dynein subunits and adaptors in mitosis reveals that dynein forms distinct complexes requiring specific recruiters and activators to promote orderly progression through mitosis.

The kinetochore localization of MPS1 is necessary for mitotic checkpoint activity and requires the microtubule-binding domain of HEC1 and the Aurora B–dependent regulation of the TPR domain.

Hook1, a microtubule and cargo tethering protein, is important for the sorting of clathrin-independent cargoes away from EEA1+ endosomes and promotes their recycling.

The BBSome, a regulator of ciliary membrane protein composition, is required only for the export phase of a process that continuously cycles phospholipase D through cilia.

The MIA complex, composed of FAP100 and FAP73, interacts with I1 dynein components and is required for normal ciliary beat frequency.

Hypoxia increases the levels of ADAM12 in a Notch-dependent manner, leading to increased ectodomain shedding of HB-EGF and subsequent promotion of invadopodia formation.

The mTOR complex 2 (mTORC2) is essential in the central nervous system for normal neuronal structure and function, potentially through effects on PKC signaling and independent of the related mTOR complex 1 (mTORC1).

Cdo-deficient mice have defects in smooth muscle fascicular reorientation during esophageal morphogenesis, resulting in structural and functional defects including an aberrantly proximal skeletal–smooth muscle boundary and achalasia.

Tools

A new immuno-TRAP technique overcomes limitations of spatial resolution and selection bias to identify gene locus associations with a nuclear subcompartment such as promyelocytic leukemia nuclear bodies.

Fluorescent lifetime imaging of an ER-tuned redox-responsive probe revealed an unanticipated stability of ER thiol redox to fluctuations in unfolded protein load, in contrast with sensitivity to lumenal calcium.

Correction

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