Cell walls (CWs) are the safeguards of plant cells and have a crucial role in controlling cell integrity and
plant-environment interactions. Perception of cell wall damage (CWD) results in activation of signaling
pathways leading to activation of plant defiance responses. Previous research utilizing murus1
GDP-L-fucose deficient mutant has shown the role of GDP-L-fucose biosynthesis in controlling the
structure and integrity of the CWs. Here, we investigated whether phenotypical consequences provoked
by the lack of GDP-L-fucose, observed in mutants lacking MURUS1 can be suppressed by blocking signal
transduction pathways involving THESEUS1 (THE1) receptor-like kinase or WALL-ASSOCIATED
KINASE 2 (WAK2)- MAP KINASE 6 (MPK6) signaling module involved in CWD responses. For this,
mur1 the1 and mur1 mpk6 double mutants were generated and analyzed. We found that the phenotypes of
double mutants closely resemble that of mur1 mutants, indicating that the morphological consequences of
GDP-L-fucose deficiency develop independently of THE1 and MPK6 signaling. Further, we aimed to
investigate whether GDP-4-keto-6-deoxymannose-3,5-epimerase-4-reductases GER1 and GER2
controlling the final step of GDP-L-fucose synthesis are functionally redundant. Due to the inability of
generating ger1 ger2 double mutants, we have applied the artificial microRNA (amiRNA) strategy to
generate ger1 ger2 amiRNA knockdown plants. We found that these knockdown plants exhibit severe
developmental growth defects similar to those observed in plants impaired in import of GDP-L-fucose
into the Golgi apparatus and these growth defects exceeded those observed in plants lacking MUR1.
Therefore, we have concluded that GER1 and GER2 are functionally redundant.
