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Secreted transforming growth factor-βs (TGF-βs) are rendered biologically inactive by binding proteins that also target and concentrate them to the extracellular matrix. Specific, but still poorly understood, activation is required for disassembly of the extracellular matrix–bound protein complex to liberate the mature growth factor and to obtain a correct biological effect. A new study shows that fibrillin-1, the protein defective in Marfan syndrome, has a biologically important role in controlling TGF-β activation in the lung.
A new study shows that cellular mRNAs can be organized and exported from the nucleus as functionally related groups by RNA-binding proteins, possibly corresponding to specific gene-expression networks activated by transcription factors. The combinatorial assortment of mRNAs as functional subsets has the potential to generate a variety of complex phenotypes from a modest number of genes.
As the caps of chromosomes, telomeres are essential for genome integrity and stability. A highly accurate method for measuring the length of a single human telomere has been developed and reveals previously unrecognized variation in telomere length.
Dyskeratosis congenita is a rare but fatal syndrome characterized by bone marrow failure. A new mouse model informs the ongoing debate on its molecular pathogenesis.
The focus of research on polycystic kidney disease (PKD) has recently shifted to the primary cilia of renal epithelial cells. A new study shows that the protein products of the genes mutated in PKD mediate mechanosensory calcium mobilization, suggesting that a disruption of fluid-flow sensing triggers abnormal cell proliferation and cyst growth.
A mouse model for familial adenomatous polyposis has been used to distinguish between possible mechanisms leading to loss of function of the Apc tumor-suppressor gene. Somatic recombination rather than chromosome loss associated with genetic instability is the primary cause of these cancers. Moreover, the data suggest that interphase nuclear architecture is a key factor in facilitating this process.
Individuals display morphological variation when genetic buffering is reduced, allowing phenotypic differences to be selected for during successive generations. A new study shows that perturbations of chromatin-inheritance genes uncover morphological variation, and epigenetic variants can be rapidly selected. This finding extends our understanding of the means by which phenotypic variation is generated and brings chromatin inheritance into the realm of multigenic traits.
The spatially and temporally coordinated interaction between migratory cardiac precursors, endothelial cells and myogenic precursors leads to the formation of the highly differentiated cell lineages in the heart. In a new study, conditional mouse mutants are used to show that Nf1 signaling in cardiac endothelium is essential for proper heart formation.
Theories of cancer biology have long held that the metastatic process originates with rare cells within the primary tumor. A new study using expression array analysis has identified a molecular signature of metastatic potential within the bulk of the primary tumor. This suggests that the majority of tumor cells have the potential to metastasize and presents exciting clinical and therapeutic applications.
