Small RNA-Seq Analysis Reveals miRNA Expression Dynamics Across Tissues in the Malaria Vector, Anopheles gambiae.

Malaria continues to be a major global health problem, where disease transmission is deeply linked to the repeated blood feeding nature of the anautogenous mosquito. Given the tight link between blood feeding and disease transmission, understanding basic biology behind mosquito physiology is a requirement for developing effective vector-borne disease control strategies. In the mosquito, numerous loss of function studies with notable phenotypes demonstrate microRNAs (miRNAs) play significant roles in mosquito physiology. While the field appreciates the importance of a handful of miRNAs, we still need global mosquito tissue miRNA transcriptome studies. To address this need, our goal was to determine the miRNA transcriptome for multiple tissues of the pre-vitellogenic mosquito. To this end, by using small RNA-Seq analysis, we determined miRNA transcriptomes in tissues critical for mosquito reproduction and immunity including (i) fat body-abdominal wall enriched tissues, (ii) midguts, (iii) ovaries, and (iv) remaining tissues comprised of the head and thorax. We found numerous examples of miRNAs exhibiting pan-tissue high- or low- expression, tissue exclusion, and tissue enrichment. We also updated and consolidated the miRNA catalog and provided a detailed genome architecture map for the malaria vector, Anopheles gambiae This study aims to build a foundation for future research on how miRNAs and potentially other small RNAs regulate mosquito physiology as it relates to vector-borne disease transmission.

Co-option during the evolution of multicellular and developmental complexity in the volvocine green algae.

Despite its major impact on the evolution of Life on Earth, the transition to multicellularity remains poorly understood, especially in terms of its genetic basis. The volvocine algae are a group of closely related species that range in morphology from unicellular individuals (Chlamydomonas) to undifferentiated multicellular forms (Gonium) and complex organisms with distinct developmental programs and one (Pleodorina) or two (Volvox) specialized cell types. Modern genetic approaches, complemented by the recent sequencing of genomes from several key species, revealed that co-option of existing genes and pathways is the primary driving force for the evolution of multicellularity in this lineage. The initial transition to undifferentiated multicellularity, as typified by the extant Gonium, was driven primarily by the co-option of cell cycle regulation. Further morphological and developmental innovations in the lineage leading to Volvox resulted from additional co-option events involving genes important for embryonic inversion, asymmetric cell division, somatic and germ cell differentiation and the structure and function of the extracellular matrix. Because of their relatively low but variable levels of morphological and developmental complexity, simple underlying genetics and recent evolutionary history, the volvocine algae are providing significant insight into our understanding of the genetics and evolution of major developmental and morphological traits.

A new class of cyclin dependent kinase in Chlamydomonas is required for coupling cell size to cell division.

Proliferating cells actively control their size by mechanisms that are poorly understood. The unicellular green alga Chlamydomonas reinhardtii divides by multiple fission, wherein a 'counting' mechanism couples mother cell-size to cell division number allowing production of uniform-sized daughters. We identified a sizer protein, CDKG1, that acts through the retinoblastoma (RB) tumor suppressor pathway as a D-cyclin-dependent RB kinase to regulate mitotic counting. Loss of CDKG1 leads to fewer mitotic divisions and large daughters, while mis-expression of CDKG1 causes supernumerous mitotic divisions and small daughters. The concentration of nuclear-localized CDKG1 in pre-mitotic cells is set by mother cell size, and its progressive dilution and degradation with each round of cell division may provide a link between mother cell-size and mitotic division number. Cell-size-dependent accumulation of limiting cell cycle regulators such as CDKG1 is a potentially general mechanism for size control.