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Inertial technology has spread widely for its comfortable use and adaptability to various motor tasks. The main objective of this study was to assess the validity of inertial measurements of the cervical spine range of motion (CROM) when compared to that of the optoelectronic system in a group of healthy individuals. A further aim of this study was to determine the optimal placement of the inertial sensor in terms of reliability of the measure, comparing measurements obtained from the same device placed at the second cervical vertebra (C2), the forehead (F) and the external occipital protuberance (EOP). Twenty healthy subjects were recruited and asked to perform flexion–extension, lateral bending, and axial rotation movements of the head. Outcome measurements of interest were CROM and mean angular velocities for each cervical movement. Results showed that inertial measurements have good reliability (0.75 < ICC < 0.9). Excellent reliability (ICC > 0.9) was found in both flexion and right lateral bending angles. All parameters extracted with EOP placement showed ICC > 0.62, while ICC < 0.5 was found in lateral bending mean angular velocities both for F and C2 placements. Therefore, the optimal sensor’s positioning emerged to be EOP. These results suggest that inertial technology could be useful and reliable for the evaluation of the CROM.

Symmetry breaking by cellular polarization is an exquisite requirement for the cell-cycle of Saccharomyces cerevisiae cells, as it allows bud emergence and growth. This process is based on the formation of polarity clusters at the incipient bud site, first, and the bud tip later in the cell-cycle, that overall promote bud emission and growth. Given the extreme relevance of this process, a surveillance mechanism, known as the morphogenesis checkpoint, has evolved to coordinate the formation of the bud and cell cycle progression, delaying mitosis in the presence of morphogenetic problems. The atypical protein kinase haspin is responsible for histone H3-T3 phosphorylation and, in yeast, for resolution of polarity clusters in mitosis. Here, we report a novel role for haspin in the regulation of the morphogenesis checkpoint in response to polarity insults. Particularly, we show that cells lacking the haspin ortholog Alk1 fail to achieve sustained checkpoint activation and enter mitosis even in the absence of a bud. In alk1Δ cells, we report a reduced phosphorylation of Cdc28-Y19, which stems from a premature activation of the Mih1 phosphatase. Overall, the data presented in this work define yeast haspin as a novel regulator of the morphogenesis checkpoint in Saccharomyces cerevisiae, where it monitors polarity establishment and it couples bud emergence to the G2/M cell cycle transition.

Haspin is a serine/threonine atypical kinase that phosphorylates histone H3-T3 during metaphase, promoting the recruitment of the chromosomal passenger complex (CPC) at kinetochores. Haspin depletion leads to cell arrest in mitosis and prevents proper chromosome positioning at the metaphase plate. Saccharomyces cerevisiae genome encodes for two haspin paralogues ALK1 and ALK2. We recently showed that these genes are essential to coordinate polarization and cell cycle progression, ensuring the correct positioning of several polarity factors following a transient mitotic delay. The aim of this project is to identify new processes where haspin kinase is involved. The first part of this work shows that Alk1 has a role at the G2/M transition in S. cerevisiae. These findings constitute the first evidence for Alk1-specific functions that are not shared by its paralogue Alk2. Our results indicate that cells lacking ALK1 are sensitive to Latrunculin A and complete nuclear division within the unbudded mother cells. These observations pointed toward a defect in the morphogenesis checkpoint. We also observed that in absence of ALK1 the Cdc28-Y19 phosphorylation signal decreases significantly during a morphogenetic stress. Exploring the underlying mechanism, we found that the decrease in phosphorylation is caused by a misregulation in Mih1 phosphatase activity in absence of Alk1. Therefore in budding yeast Alk1 modulates G2/M cell cycle switch by regulating Mih1 3 activity. The second part of this work is focused on exploring the role of Alk1 and Alk2 in polarisome dispersion. We show that the previously reported role of haspin in polarization relies on its ability to modulate Ras localization. Our observations are indicative for a mitotic role of Ras, which, by regulating Cdc24 redistribution, influences Cdc42 activation at polarized sites. These observations may help to shed light on alterations in cell polarity, which often constitute the molecular mechanism for cancer insurgence.

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