Response of the Atmosphere to Orographic Forcings: Insight from Idealised Simulations

Earth’s orography profoundly influences its climate and is a major reason behind the zonally asymmetric features observed in the atmospheric circulation. The response of the atmosphere to orographic forcing, when idealized aqua mountains are placed individually and in pairs (180° apart) at different latitudes, is investigated in the present study using a simplified general circulation model. The investigation reveals that the atmospheric response to orography is dependent on its latitudinal position: orographically triggered stationary waves in the mid-latitudes are most energetic compared to the waves generated due to anomalous divergence in the tropics. The impact on precipitation is confined to the latitude of the orography when it is placed near the tropics, but when it is situated at higher latitudes, it also has a significant remote impact on the tropics. In general, the tropical mountains block the easterly flow, resulting in a weakening of the Hadley cells and a local reduction in the total poleward flux transport by the stationary eddies. On the other hand, the mid-latitudinal orography triggers planetary-scale Rossby waves and enhances the poleward flux transport by stationary eddies. The twin mountains experiments, which are performed by placing orography in pairs at different latitudes, show that the energy fluxes, stationary wave, and precipitation pattern are not merely the linear additive sum of individual orographic responses at these latitudes. The non-linearity in a diagnostic sense is a product interaction of flow between the two mountains, which depends on the background flow, the separation distance between mountains, and wind shear worldwide.

Sliding of kinetochore fibers along bridging fibers helps center the chromosomes on the spindle

ABSTRACTChromosome alignment at the spindle equator during metaphase is the most remarkable feature of mitosis, which promotes proper chromosome segregation and depends on the forces exerted at the plus end of kinetochore microtubules and polar ejection forces. However, forces arising from lateral mechanical coupling of kinetochore fibers with non-kinetochore microtubules play a role in chromosome alignment, but the mechanism is unclear. Here we develop a speckle microscopy assay to measure the poleward flux of individual microtubules in spindles of human cells and show that bridging microtubules slide apart and undergo poleward flux at a higher rate than kinetochore microtubules. Depletion of the microtubule coupler NuMa increased the difference in the flux velocity of kinetochore and bridging microtubules, suggesting that sliding forces from the bridging fiber are transmitted largely through NuMa onto the associated kinetochore fibers. Depletions of Kif18A/kinesin-8, Kif4A/kinesin-4, as well as double depletions of Kif18A together with Kif4A or Kif18A together with the crosslinker of antiparallel microtubules PRC1 increased the flux velocity of kinetochore fibers up to the velocity of bridging fibers, due to the increased coupling resulting from the extended antiparallel overlap regions. We found severe kinetochore misalignment after double Kif18A and Kif4A as well as Kif18A and PRC1 depletions compared to a single Kif18A depletion, suggesting that forces within the bridging fiber have a centering effect on the kinetochores. We propose that lateral length-dependent sliding forces that the bridging fiber exerts onto kinetochore fibers drive the movement of kinetochores towards the spindle center, thereby promoting chromosome alignment.

Augmin regulates kinetochore tension and spatial arrangement of spindle microtubules by nucleating bridging fibers

ABSTRACTThe mitotic spindle functions as a molecular micromachine that evenly distributes chromosomes into two daughter cells during cell division. Spindle microtubules in human cells are mainly nucleated at the centrosome and on the lateral surface of existing microtubules by the augmin complex. However, it is unknown how the augmin-mediated nucleation affects functionally distinct microtubule bundles and consequently the forces within the spindle. Here we show, by using siRNA depletion and CRISPR knock-out of the augmin complex subunits HAUS6 or HAUS8, that augmin is crucial for the nucleation of bridging microtubules, which laterally link sister kinetochore fibers. Augmin depletion resulted in a reduction in the number of microtubules within bridging fibers by around 80% and in kinetochore fibers by 40%, suggesting that the bridging microtubules are mainly nucleated at the surface of present microtubules. In augmin-depleted cells, the interkinetochore distance decreased preferentially for kinetochores that lack a bridging fiber, independently of the thickness of their k-fibers, implying that augmin affects forces on kinetochores largely via bridging fibers. Without augmin the number of bridging fibers decreased, with the remaining ones mostly confined to the spindle periphery with an increased overlap length. A slower poleward flux of microtubules after augmin depletion is indicative of slower sliding within the bridging fiber. Our results demonstrate a critical role of augmin in the formation of bridging microtubules and proper architecture of the metaphase spindle, suggesting a model where sliding of augmin-nucleated bridging microtubules promotes poleward flux of k-fibers and thus tension on kinetochores.

Microtubule poleward flux in human cells is driven by the coordinated action of four kinesins

Mitotic spindle microtubules (MTs) undergo continuous poleward flux, whose driving force and function in humans remain unclear. Here, we combined loss-of-function screenings with analysis of MT dynamics in human cells to investigate the molecular mechanisms underlying MT-flux. We report that kinesin-7/CENP-E at kinetochores (KTs) is the predominant driver of MT-flux in early prometaphase, while kinesin-4/KIF4A on chromosome arms facilitates MT-flux during late prometaphase and metaphase. We show that both of these activities work in coordination with MT-crosslinking motors kinesin-5/EG5 and kinesin-12/KIF15. Our data further indicate that MT-flux driving force is transmitted from non-KT MTs to KT-MTs via MT-coupling by HSET and NuMA. Moreover, we found that MT-flux rate correlates with spindle size and this correlation depends on the establishment of stable end-on KT-MT attachments. Strikingly, we revealed that flux is required to counteract the kinesin 13/MCAK-dependent MT-depolymerization to regulate spindle length. Thus, our study demonstrates that MT-flux in human cells is driven by the coordinated action of four kinesins, and is required to regulate mitotic spindle size in response to MCAK-mediated MT-depolymerizing activity at KTs.