Advances in Anatomy Embryology and Cell Biology最新文献

Cellular polarization involves significant remodeling and decentralization of the nucleus-associated centrosome to focal points at the apical and basolateral surfaces which is associated with major remodeling of the microtubule system in which individual microtubules become nucleated and organized from the polarizing cell surfaces, as studied in polarizing epithelial cells (reviewed in Müsch 2004; Muroyama and Lechler 2017). These changes are associated with cellular asymmetry in preparation for cellular differentiation of previously non-committed cells. During this process, the previously nucleus-associated centrosome becomes deconstructed into specific centrosomal components which are now referred to as "non-centrosomal." At the present time we still only have limited information about this process and to understanding the mechanisms underlying the centrosome decentralization process. Gaining detailed insights is further complicated by the fact that there is considerable diversity in the molecular mechanisms of centrosome and microtubule reorganization.

Among the multiple and intriguing roles of centrosomes in cellular functions is the ubiquitin-proteasome-mediated protein degradation. It has been shown that proteasomes are concentrated at the mammalian centrosome which led to further studies to view the centrosome as a proteolytic center (Wojcik et al. 1996; Wigley et al. 1999; reviewed in Badano et al. 2005). Proteasomal components that are concentrated around the centrosome include ubiquitin, the 20S and 19S subunits of the proteasome, as well as the E3 enzyme parkin. These proteasomal components colocalize with the centrosomal marker γ-tubulin and co-purify with γ-tubulin in the centrosomal fractions after sucrose-gradient ultracentrifugation (Wigley et al. 1999). The localization, accumulation, and concentration of proteasomal components around centrosomes appear to be microtubule independent which has been shown experimentally by inhibiting microtubule functions. When intracellular levels of misfolded proteins were experimentally increased by either proteasome inhibition with drugs such as lactacystin, or by overexpression of misfolded mutant proteins, the centrosome-associated proteasome network became expanded and proteolytic components were recruited from the cytosol without involvement of microtubules. These studies revealed a critical role of centrosomes in the organization and subcellular localization of proteasomes (Wigley et al. 1999; Fabunmi et al. 2000).

It is well known that plant cells do not contain typical centrosomes and the question has been asked how plant cells undergo mitosis and cell division in the absence of mechanisms that are well known for eukaryotic animal cells. Several papers are now available to address this question.

The centrosome field has seen enormous progress during the past few decades which spans the large areas of cell biology with new information on cell cycle controls and cellular health; immunology with centrosomes being essential for the formation of the immunological synapse; neurobiology with new insights into centrosome dysfunctions leading to disorders and disease; stem cell biology with fate-determining distribution of centrosomal material during asymmetric cell division; cancer biology with huge insights into the role of centrosomes in disease initiation, progression, and manifestation; reproductive biology with essential centrosome functions in oocytes, during fertilization and embryo development in which centrosome dysfunctions can be related back to abnormal centrosomal material in the meiotic spindle of oocytes; and several others that will be highlighted in the specific chapters of this book.

One of the most interesting aspects of host cell-viral interactions is how the pathogen exploits the host cell cytoskeleton and centrosomes for survival in the host cell.

Stem cells are important to sustain tissue growth during development, to repair damaged tissue after injury, and to maintain homeostasis during adulthood. Precisely programmed stem cell renewal and differentiation is critical, as failure in balance can lead to tumorigenesis as a result of over-proliferation or to degeneration as a result of decline in stem cell functions (reviewed in Roth et al (2012); Chen et al (2021).

In the vertebrate tree of life, viviparity or live birth has independently evolved many times, resulting in a rich diversity of reproductive strategies. Viviparity is believed to be a mode of reproduction that evolved from the ancestral condition of oviparity or egg laying, where most of the fetal development occurs outside the body. Today, there is not a simple model of parity transition to explain this species-specific divergence in modes of reproduction. Most evidence points to a gradual series of evolutionary adaptations that account for this phenomenon of reproduction, elegantly displayed by various viviparous squamates that exhibit placentae formed by the appositions of maternal and embryonic tissues, which share significant homology with the tissues that form the placenta in therian mammals. In an era where the genomes of many vertebrate species are becoming available, studies are now exploring the molecular basis of this transition from oviparity to viviparity, and in some rare instances its possible reversibility, such as the Australian three-toed skink (Saiphos equalis). In contrast to the parity diversity in squamates, mammals are viviparous with the notable exception of the egg-laying monotremes. Advancing computational tools coupled with increasing genome availability across species that utilize different reproductive strategies promise to reveal the molecular underpinnings of the ancestral transition of oviparity to viviparity. As a result, the dramatic changes in reproductive physiology and anatomy that accompany these parity changes can be reinterpreted. This chapter will briefly explore the vertebrate modes of reproduction using a phylogenetic framework and where possible highlight the role of potential candidate genes that may help explain the polygenic origins of live birth.

Chapter 8 was inadvertently published with errors and the following corrections were updated.