DG-algebras and derived A-infinity algebras

A differential graded algebra can be viewed as an A-infinity algebra. By a theorem of Kadeishvili, a dga over a field admits a quasi-isomorphism from a minimal A-infinity algebra. We introduce the notion of a derived A-infinity algebra and show that any dga A over an arbitrary commutative ground ring k is equivalent to a minimal derived A-infinity algebra. Such a minimal derived A-infinity algebra model for A is a k-projective resolution of the homology algebra of A together with a family of maps satisfying appropriate relations. As in the case of A-infinity algebras, it is possible to recover the dga up to quasi-isomorphism from a minimal derived A-infinity algebra model. Hence the structure we are describing provides a complete description of the quasi-isomorphism type of the dga.Comment: v3: 27 pages. Minor corrections, to appear in Crelle's Journa

The Diversification of the LIM Superclass at the Base of the Metazoa Increased Subcellular Complexity and Promoted Multicellular Specialization

Background: Throughout evolution, the LIM domain has been deployed in many different domain configurations, which has led to the formation of a large and distinct group of proteins. LIM proteins are involved in relaying stimuli received at the cell surface to the nucleus in order to regulate cell structure, motility, and division. Despite their fundamental roles in cellular processes and human disease, little is known about the evolution of the LIM superclass. Results: We have identified and characterized all known LIM domain-containing proteins in six metazoans and three nonmetazoans. In addition, we performed a phylogenetic analysis on all LIM domains and, in the process, have identified a number of novel non-LIM domains and motifs in each of these proteins. Based on these results, we have formalized a classification system for LIM proteins, provided reasonable timing for class and family origin events; and identified lineagespecific loss events. Our analysis is the first detailed description of the full set of LIM proteins from the non-bilaterian species examined in this study. Conclusion: Six of the 14 LIM classes originated in the stem lineage of the Metazoa. The expansion of the LIM superclass at the base of the Metazoa undoubtedly contributed to the increase in subcellular complexity required for the transition from a unicellular to multicellular lifestyle and, as such, was a critically important event in the history of animal multicellularity

Logarithmic topological Hochschild homology of topological K-theory spectra

Contains fulltext : 183369.pdf (preprint version ) (Open Access

Targeted disruption of the mouse Csrp2 gene encoding the cysteine-and glycine-rich LIM domain protein CRP2 result in subtle alteration of cardiac ultrastructure

Background: The cysteine and glycine rich protein 2 (CRP2) encoded by the Csrp2 gene is a LIM domain protein expressed in the vascular system, particularly in smooth muscle cells. It exhibits a bimodal subcellular distribution, accumulating at actin-based filaments in the cytosol and in the nucleus. In order to analyze the function of CRP2 in vivo, we disrupted the Csrp2 gene in mice and analysed the resulting phenotype. Results: A similar to 17.3 kbp fragment of the murine Csrp2 gene containing exon 3 through 6 was isolated. Using this construct we confirmed the recently determined chromosomal localization (Chromosome 10, best fit location between markers D10Mit203 proximal and D10Mit150 central). A gene disruption cassette was cloned into exon 4 and a mouse strain lacking functional Csrp2 was generated. Mice lacking CRP2 are viable and fertile and have no obvious deficits in reproduction and survival. However, detailed histological and electron microscopic studies reveal that CRP2-deficient mice have subtle alterations in their cardiac ultrastructure. In these mice, the cardiomyocytes display a slight increase in their thickness, indicating moderate hypertrophy at the cellular level. Although the expression of several intercalated disc-associated proteins such as beta-catenin, N-RAP and connexin-43 were not affected in these mice, the distribution of respective proteins was changed within heart tissue. Conclusion: We conclude that the lack of CRP2 is associated with alterations in cardiomyocyte thickness and hypertroph