Lintless mutant is a super-short fiber mutant in upland cotton only 4—8 mm in fiber length and also named Ligon cotton controlled by one dominant gene Li1. Fiber ul- trastructure of the mutant (Li1) and its wild type (li1) in situ and in vitro was observed under an electron microscope to understand its cytological characteristics during the fiber cell elongation. The results showed that the mutant fiber in situ had thinner cytoplasm, more small vacuoles, less mitochon- dria, Golgi apparatus and endoplasmic reticula, and there were more starch granules which were free or packed in the amyloplast beside the cell wall than that of wild type. It was indicated that scarcity of functional organelles and disability of transformation from starch to sugar might be associated with the fact that the mutant fiber cell was aborted too early to elongate into normal length. Mutant ovule in some media containing GA3 could produce a kind of huge callus that grew faster than normal ovules. The callus was covered with many white, loose, and semitransparent fiber-like cells that apt to get off from ovule. These fiber-like cells were multi- cellular fibers generated by cell division and had black dots just like pigment glands in the stem and leaf of cotton. There were lots of micro-tubes beside cytoplasm membrane of the multicellular fiber, which were thought to be primary preparation for second wall deposition of multicellular fiber. It was indicated that GA3 might induce the expression of gene(s) that kept inactive in the field condition and then stimulate the original fiber cell in vitro to undergo division again. Lintless mutant is a super-short fiber mutant in upland cotton only 4-8 mm in fiber length and also named Ligon cotton controlled by one dominant gene Li1. Fiber ul-trastructure of the mutant (Li1) and its wild type (li1) in situ and in vitro was observed under an electron microscope to understand its cytological characteristics during the fiber cell elongation. The results showed that the mutant fiber in situ had thinner cytoplasm, more small vacuoles, less mitochon- dria, Golgi apparatus and endoplasmic reticula, and there were more starch granules which were free or packed in the amyloplast beside the cell wall than that of wild type. It was indicated that scarcity of functional organelles and disability of transformation from starch to sugar might be associated with the fact that the mutant fiber cell was aborted too early early to elongate into normal length. Mutant ovule in some media containing GA3 could produce a kind of huge callus that grew faster than normal ovu les. The callus was covered with many white, loose, and semitransparent fiber-like cells that apt to get off from ovule. These fiber-like cells were multi-cellular fibers generated by cell division and had black dots just like pigment glands in the stem and leaf of cotton. There were lots of micro-tubes beside cytoplasm membrane of the multicellular fiber, which were thought to be primary preparation for second wall deposition of multicellular fiber. It was indicated that GA3 might induce the expression of gene (s) that kept inactive in the field condition and then stimulate the original fiber cell in vitro to undergo division again.