Results show that (i) ChlSPAD and FM decreased concurrently with the onset and time development of foliar injury (suggesting a degradation of chlorophyll due to an excess of the total oxidative stress), with a much stronger reduction when the injury becomes widespread (reduction of chlorophyll due to increased necrotic surface).
Combined Hoxd1 and XMeis3 loss-of-function also indicates synergy; while sub optimal amounts of either morpholino against Hoxd1 or XMeis3 led to a reduction of Hoxd1 expression, the combination led to a much stronger reduction.
On the other hand, the Western blot data indicates a much stronger reduction of around 90% (contradicting the flow cytometry data somewhat).
In Sgca-; Sgce-null skeletal and cardiac muscle, there was a much stronger reduction in dystrophin and dystroglycan expression compared with that of Sgca-null mice.
Similarly, an almost two-fold reduction of promoter-proximal paused and elongating Pol II was seen at all expressed genes, with a much stronger reduction at down-regulated genes.
α-dystroglycan, β-dystroglycan and dystrophin were also reduced in comparison to wild-type animals, but, interestingly, the Sgca-; Sgce-null mice dystrophin showed a much stronger reduction compared with the Sgca-null mice in which it is already reduced.
In comparison, the more specific compound PP2 that only inhibits the Src family of tyrosine kinases caused a much stronger reduction in cell number, in particular at the 10 μmol/l concentration.
Cultivation of plants under low P conditions, caused a much stronger reduction of photosynthetic capacity of the leaves, and C assimilation as well as effective PSII fluorescence were reduced to 50% or 45% respectively (Table 2).
In our experiments the inhibition of monocyte recruitment to the subretinal space in Cx3cr1 −/− mice (Ccl2, Ccr2 deletion and monocyte depletion, Figs 3 and 5) resulted in a 50% reduction of subretinal MP accumulation, but in a much stronger reduction of photoreceptor cell death (Figs 4 and 5).
In this case, we observed a much stronger reduction in pairing of the 359 bp repeat relative to dsRNAs targeting Pr-set7 (Table 3), in line with our reasoning that loss of Pr-set7 has a modest effect on somatic homolog pairing in comparison with our 17 FISH hits.
