The anther generally has four lobes and each lobe contains reproductive microsporocyte surrounded by various layers of somatic cells viz., tapetum, middle layer, endothecium, and epidermis. In Arabidopsis, multiple LRR-RLKs like excess microsporocytes1 (EMS1)/extra sporogenous cell (EXS), somatic embryogenesis receptor-like kinase 1/2 (SERK1/2), receptor-like protein kinase 2 (RPK2), barely any meristem 1/2 (BAM1/2), CLAVATA3 insensitive receptor kinase (CIK1/2/3/4), ERECTA (ER), and ERECTA-like 1/2 (ERL1/2) regulate anther development, especially, the differentiation and patterning of the somatic cell layers. EMS1/EXS was the first LRR-RLK to be identified that plays a crucial role in anther cell differentiation [
82,
83]. The anthers of
ems1/exs mutants lack tapetum but produce large numbers of microsporocytes than the wild type. In addition, delayed expression of
EMS1 in the
ems1 mutant tapetal initials has been shown to aid in the generation of a functional tapetum and the diminution of microsporocyte numbers [
84]. These results suggest that EMS1/EXS determines the fate of tapetal cells during early anther development. Tapetum determinant 1 (TPD1), a small secreted protein, is known to induce the phosphorylation of EMS1/EXS, thus, behaving as their ligand; and the signal is transduced downstream via phosphorylation of β-carbonic anhydrases (βCAs) [
85,
86]. Similarly, SERK1/2 has also been known to determine tapetal cell fate, as the anthers of
serk1serk2 double mutants are phenotypically similar to that of
ems1/exs mutant [
18,
87]. Moreover, SERK1 interacts with and transphosphorylates EMS1 to enhance its activity for guiding a co-regulatory network (A) [
88]. Corroborated by the phenotype of
rpk2 mutants, it can be deduced that RPK2 is responsible for the differentiation of middle layers and tapetum during anther development. It essentially controls tapetal cell fate by triggering their degradation via modulation of the enzymes involved in cell wall metabolism and lignin biosynthesis [
89] (A). Both BAM1 and BAM2 are responsible for regulating early stages of anther differentiation, as confirmed by the lack of somatic cell layers, including endothecium, middle layer, and tapetum in
bam1bam2 double mutants [
90]. CLAVATA3 insensitive receptor kinases (CIK1/2/3/4) are co-receptors of BAM1/2 and RPK2, which regulate the determination of parietal cell fate and archesporial cell division [
91] (A). ERECTA (ER), ERECTA-Like 1 (ERL1), and ERL2 are also known to play essential roles in healthy anther lobe formation and anther cell differentiation via mitogen-activated protein kinases like MPK3/MPK6 (A). The sterility of
er-105 erl1-2 erl2-1 triple mutant and the phenotypic similarity of the anther lobes in single mutants of
er-105 or
erl1-2 or
erl2-1 with that of
mpk3 or
mpk6 mutants suggests the correlation of these genes in the regulation of anther cell division and differentiation [
92]. Further, a Lectin RLK, small, glued together, collapsed (SGC) has also been validated as a regulator of pollen development as its knockout had led to the development of small, glued-together and collapsed pollen and resulted in male sterility [
93] (A).
Knowledge about the role of RLKs in ovule development is very scarce. In Arabidopsis ovules,
EMS1 is expressed in nucellar epidermis and chalaza, while
TPD1 is weakly restricted to the distal end of integuments. Altered expression of cell-cycle genes and auxin signaling genes during ovule development, concomitant with the ectopic expression of
TPD1, indicates the regulation of ovule development by TPD1-EMS1 [
94] (A).