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The anterior visceral endoderm (AVE) plays an important role in anterior–posterior axis formation in the mouse. The AVE functions in part by expressing secreted factors that antagonize growth factor signaling in the proximal epiblast. Here we report that the Secreted frizzled-related protein 5 (Sfrp5) gene, which encodes a secreted factor that can antagonize Wnt signaling, is expressed in the AVE and foregut endoderm during early mouse development. At embryonic day (E) 5.5, Sfrp5 is expressed in the visceral endoderm at the distal tip region of the embryo and at E6.5 in the AVE opposite the primitive streak. In Lim1 embryos, which lack anterior neural tissue and sometimes form a secondary body axis, Sfrp5-expressing cells fail to move towards the anterior and remain at the distal tip of E6.5 embryos. When compared with Dkk1, which encodes another secreted Wnt antagonist molecule present in the visceral endoderm, Sfrp5 and Dkk1 expression overlap but Sfrp5 is expressed more broadly in the AVE. Between E7.5 and 8, Sfrp5 is expressed in the foregut endoderm underlying the cardiac mesoderm. At E8.5, Sfrp5 is expressed in the ventral foregut endoderm that gives rise to the liver. Additional domains of Sfrp5 expression occur in the dorsal neural tube and in the forebrain anterior to the optic placode. These findings identify a gene encoding a secreted Wnt antagonist that is expressed in the extraembryonic visceral endoderm and anterior definitive endoderm during axis formation and organogenesis in the mouse. [Copyright &y& Elsevier]

Candida albicans, the most prevalent fungal pathogen of humans, grows with multiple morphologies. The dynamics of nuclear movement are similar in wild-type yeast and pseudohyphae: nuclei divide across the bud neck. By contrast, in hyphae, nuclei migrate 10-20 µm into the growing germ tube before dividing. We analyzed the role of the dynein-dynactin complex in hyphal and yeast cells using time-lapse fluorescence microscopy. Cells lacking the heavy chain of cytoplasmic dynein or the p150Glued subunit of dynactin were defective in the position and orientation of the spindle. Hyphal cells often failed to deliver a nucleus to the daughter cell, resulting in defects in morphogenesis. Under yeast growth conditions, cultures included a mixture of yeast and pseudohyphal-like cells that exhibited distinctive defects in nuclear dynamics: in yeast, nuclei divided within the mother cell, and the spindle position checkpoint protein Bub2p ensured the delivery of the daughter nucleus to the daughter cell before cytokinesis; in pseudohyphal-like cells, pre-mitotic nuclei migrated into the daughter and no checkpoint ensured return of a nucleus to the mother cell before cytokinesis. Analysis of double mutants indicated that Bub2p also mediated the pre-anaphase arrest and polarization of pseudohyphal-like cells. Thus, Bub2p has two distinct roles in C. albicans cells lacking dynein: it mediates pre-anaphase arrest and it coordinates spindle disassembly with mitotic exit. [ABSTRACT FROM AUTHOR]

The article presents a study which shows that the morphogenesis checkpoint kinase Swe1 influences a cell cycle delay causing growth defects in Candida albicans and Saccharomyces cerevisiae cells without CaSLA2 or ScSLA2 endocytic patch protein. It says that the study compared actin organization and cell cycle dynamics in strains without Sla1 and Abp1 to those in strains without Sla2. It reveals that of all strains with Swe1-dependent phenotypes, only sla2 strains are defective in actin cables.