Similarly, Danon diseases, characterized by cardiomyopathy and myopathy, are associated with the failure of autophagosome to fuse with lysosome.
Further demonstration of the failure of autophagosomes to fuse with lysosomes in La2O3 or CQ-treated THP-1 cells was provided by confocal microscopy, which failed to demonstrate colocalization of the accumulated GFP-LC3 complexes with LAMP-1+ lysosomes.
In striking contrast, the failure of phagosomes to fuse with lysosomes is a frequent finding following macrophage ingestion of Mycobacterium tuberculosis (MTB) and the variant M. bovis BCG, enabling these organisms to reside safely in vacuoles that support their survival and replication [ 31, 32, 47].
One of them is Mycobacterium tuberculosis (Mtb) whose resistance to early mechanisms of macrophage killing and failure of its phagosomes to fuse with lysosomes causes tuberculosis (TB) disease in humans.
Since KIF5B functions as a plus-end motor, i.e. a motor that transports cargo from the centrosome to the cell periphery [24], the accumulation of lysosomes to the cell periphery in KIF5B-depleted cells could be due to a peripheral localization of the centrosome or a failure of the lysosomes to fuse with the plasma membrane.
Twinning has been associated with a high peri-natal mortality rate and MZ twins display a higher prevalence of congenital abnormalities, many of which appear to be related to failure of bilateral structures to fuse properly during development.
Taken together, these data support the idea that the failure of the prominences to fuse and form a normal primary palate is a direct effect of the change in shape.
These include defective autophagosome synthesis (Aguado et al, 2010), loss of autophagosomes' ability to recognize damaged mitochondria or other organelles (Martinez-Vicente et al, 2010; Khalil et al, 2015), and failure of the autophagosomes to fuse with lysosomes (Martinez-Vicente et al, 2010; Wong & Holzbaur, 2014).
