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Simple Summary: The biology of cellular senescence has broad implications for the fields of aging, tissue and wound repair, tumor biology, and development. Cellular senescence is a state of irreversible growth arrest, which is induced by internal and external stress mechanisms. Senescent cell populations are diverse and display transcriptomic and biomolecular variability, making it difficult to find a sole specific biomarker from defining this state. Although this cell fate is involved in cutaneous wound healing and tissue repair, there is still a substantial gap in understanding how senescent cells modulate regenerative processes. Addressing remaining key questions in the field may guide clinical care and management of both acute and chronic wounds and the development of novel therapeutic agents. Cellular senescence has gained increasing attention in the field of aging research. Senescent cells have been implicated in biological aging processes, tumorigenesis, development, and wound repair amongst other processes and pathologies. Recent findings reveal that senescent cells can both promote and inhibit cutaneous wound healing processes. Relating senescent cells in acute and chronic wounds will help to clarify their role in wound healing processes and inform our understanding of senescent cell heterogeneity. To clarify this apparent contradiction and guide future research and therapeutic development, we will review the rapidly growing field of cellular senescence and its role in wound healing biology. [ABSTRACT FROM AUTHOR]

Flightin is a myosin binding protein present in Pancrustacea. In Drosophila, flightin is expressed in the indirect flight muscles (IFM), where it is required for the flexural rigidity, structural integrity, and length determination of thick filaments. Comparison of flightin sequences from multiple Drosophila species revealed a tripartite organization indicative of three functional domains subject to different evolutionary constraints. We use atomic force microscopy to investigate the functional roles of the N-terminal domain and the C-terminal domain that show different patterns of sequence conservation. Thick filaments containing a C-terminal domain truncated flightin (flnΔC44) are significantly shorter (2.68 ± 0.06 µm; p < 0.005) than thick filaments containing a full length flightin (fln; 3.21 ± 0.05 µm) and thick filaments containing an N-terminal domain truncated flightin (flnΔN62; 3.21 ± 0.06 µm). Persistence length was significantly reduced in flnΔN62 (418 ± 72 µm; p < 0.005) compared to (fln (1386 ± 196µm) and flnΔC44 (1128 ± 193 µm). Statistical polymer chain analysis revealed that the C-terminal domain fulfills a secondary role in thick filament bending propensity. Our results indicate that the flightin amino and carboxy terminal domains make distinct contributions to thick filament biomechanics. We propose these distinct roles arise from the interplay between natural selection and sexual selection given IFM's dual role in fiight and courtship behaviors. [ABSTRACT FROM AUTHOR]