Catalyzes the hydrolysis of ester bond in chlorophyll to yield chlorophyllide and phytol (PubMed:10611389, PubMed:11950974). Shows a preferential activity toward chlorophyll a (PubMed:11950974). Does not seem to be required for chlorophyll degradation during senescence (PubMed:17996203, PubMed:18349515, PubMed:31779896). May modulate the balance between different plant defense pathways (PubMed:15598807). a chlorophyll + H2O = a chlorophyllide + H(+) + phytol chlorophyll a + H2O = chlorophyllide a + H(+) + phytol Porphyrin-containing compound metabolism; chlorophyll degradation. Expressed in seedlings, leaves, flowers and siliques, but not in roots. Constitutively expressed in flowers with a higher level at the stage of buds. Induced by methyl jasmonate, coronatine, a phytotoxin produced by some plant-pathogenic bacteria or rapidly after wounding, with a peak after 30 minutes and a return to the basal level in the following 4 hours (PubMed:9501136). Induced by methyl jasmonate (JA), wounding, infection with the bacterial pathogen Pectobacterium carotovorum, and with the fungal pathogen Alternaria brassicicola (PubMed:15598807). Induced by transition from dark to white light (PubMed:21896889). Down-regulated by dark (PubMed:21896889). It has been proposed that some chlorophyllase might be transported to vacuole via the endoplasmic reticulum where they might be glycosylated (Probable). Unlike CLH2, the expression of this protein is dependent on the presence of a functional COI1 protein (PubMed:11950974). Plants silencing CLH1 exhibit reduced size, and decreased levels of chlorophyll and chlorophyllide (PubMed:15598807). Plants silencing CLH1 exhibit enhanced resistance and salicylate (SA) levels, and decreased jasmonate levels (JA) upon infection with the bacterial pathogen Pectobacterium carotovorum (PubMed:15598807). Plants silencing CLH1 exhibit enhanced susceptibility to infection by the fungal pathogen Alternaria brassicicola (PubMed:15598807). Belongs to the AB hydrolase superfamily. Lipase family.