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. Author manuscript; available in PMC: 2014 Jan 25.
Published in final edited form as: Brain Struct Funct. 2009 Dec 11;214(0):263–283. doi: 10.1007/s00429-009-0235-3

Table 2.

Overexpression of C. elegans proteins implicated in AD

C. elegans protein C. elegans promoter Expression in C. elegans Fold over-expression Rescuing ability & phenotypes Transgene name/(plasmid) References
Endogenous expression of APL-1
APL-1 apl-1 head and tail neurons, ventral cord, hypodermis and supporting cells, vulva muscles 125x rescues apl-1 null lethality; low level (5.5%) L1 lethality; reduced brood size; sluggish ynIs86 (Hornsten et al. 2007)
APL-1::GFP 180x rescues apl-1 null lethality; high level (70%) L1 lethality and morphological defects; cell and organ detachment; reduced brood size; sluggish ynIs79 (Hornsten et al. 2007)
APL-1 extracellular domain rescues apl-1 null lethality; slowed development; reduced brood size; sluggish ynIs71, ynEx106, ynIs106A (Hornsten et al. 2007)
APL-1ΔGoa rescues apl-1 null lethality (Hornsten et al. 2007)
APL-1ΔE1b rescues apl-1 null lethality (Hornsten et al. 2007)
APL-1ΔE2c rescues apl-1 null lethality (Hornsten et al. 2007)
APL-1ΔE1-E2d no rescue of apl-1 null lethality (Hornsten et al. 2007)
Neuronal expression of APL-1
APL-1 snb-1 constitutively in all neurons; pharynx; arcade cells; distal tip cell; vulval muscle; spermatheca; gonad sheath cells; body wall muscle; hypodermis; seam cellse 71x and 17x respectively rescues apl-1 null lethality; reduced brood size; sluggishness ynIs12, ynIs13 (Hornsten et al. 2007)
APL-1 extracellular domainf rescues apl-1 null lethality ynEx166 (Hornsten et al. 2007)
APL-1::GFP rab-3 constitutively in all neurons rescues apl-1 null lethality (Hornsten et al. 2007)
Expression of Proteins in the γ-secretase complexg
SEL-12 sel-12 constitutively in most cell types, except intestine rescues sel-12 null phenotypes byIs100, byIs101, SEL-12 (Levitan et al. 1996; Wittenburg et al. 2000)
SEL-12 ttx-3 only in AIY neuron rescues sel-12 null phenotypes (pBY478) (Wittenburg et al. 2000)
SEL-12 egl-13 Pi cell, neurons, bodywall muscles, intestine partially rescues egg laying defect and Pi cell fate of sel-12 null worms (cHNC2) (Cinar et al. 2001)
HOP-1 sel-12 constitutively in most cell types, except intestine rescues sel-12 null phenotypes HOP-1 (Li and Greenwald 1997)
APH-1 sel-12 constitutively in most cell types, except intestine rescues egg laying defect of aph-1 null worms (Note: no rescue under aph-1 endogenous promoter) Ce3aph-1 (Francis et al. 2002)
PEN-2 pen-2 neurons, muscles, intestine, vulva rescues egg laying defect of pen-2 null worms pen-2 genomic (Francis et al. 2002)
PEN-2 sel-12 constitutively in most cell types, except intestine rescues egg laying defect of pen-2 null worms Ce pen-2 (Francis et al. 2002)
Endogenous expression of the α-secretase
ADM-4 adm-4 pharynx, intestine, tail rescues sterility of sup-17; adm-4 double mutants arEx399, arEx400 (Jarriault and Greenwald 2005)
a

APL-1ΔGo: deletion of Go-binding sequence

b

APL-1ΔE1: deletion of E1 domain

c

APL-1ΔE2: deletion of E2 domain

d

APL-1ΔE1-E2: deletion of E1 through E2 domains

e

Expression pattern of Psnb-1::GFP (BC11116; Hunt-Newbury et al. 2007)

f

APL-1EXT: the entire extracellular domain of APL-1. APL-1EXT is not further cleaved and is slightly larger than sAPL-1

g

No rescue of maternal effect lethal phenotype for aph-1, aph-2, pen-2, probably due to co-suppression of their endogenous locus in the germline, a general germline effect described in Dernburg et al. (2000)