We have identified a 60 kDa membrane protein (MP60) as a component of
the mouse cortical lens fiber gap junction and a monoclonal antibody r
ecognizing this protein has been used to establish the temporal and sp
atial patterns of gap junction formation during development of the mou
se lens. The initial expression of MP60 during embryonic development o
f the mouse lens correlates with primary fiber elongation and is first
seen on the luminal aspect of the extending cells. About 2 days after
birth, the relatively large, antibody-positive macular structures cha
racteristic of late embryonic fiber cells begin to disperse into progr
essively smaller structures within a centrally located region of the l
ens. This change in the staining pattern with antibody directed agains
t MP60 is consistent with the dispersion of gap junction plaques as co
nfirmed by freeze fracture analysis. Around 5 days after birth, the 60
kDa gap junctional protein in this central region of the lens undergo
es a modification resulting in the alteration to the epitope for the m
onoclonal antibody and a consequent loss of immunorecognition. Our res
ults suggest that gap junctions in the central region of the developin
g mouse lens undergo sequential changes in immunoreactivity which may
reflect potentially distinct functional phases of intercellular commun
ication.